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<journal-id journal-id-type="publisher-id">Front. Physiol.</journal-id>
<journal-title>Frontiers in Physiology</journal-title>
<abbrev-journal-title abbrev-type="pubmed">Front. Physiol.</abbrev-journal-title>
<issn pub-type="epub">1664-042X</issn>
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<publisher-name>Frontiers Media S.A.</publisher-name>
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<article-id pub-id-type="publisher-id">1392454</article-id>
<article-id pub-id-type="doi">10.3389/fphys.2024.1392454</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Physiology</subject>
<subj-group>
<subject>Review</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group>
<article-title>A bibliometric analysis of endoplasmic reticulum stress and atherosclerosis</article-title>
<alt-title alt-title-type="left-running-head">Huang et al.</alt-title>
<alt-title alt-title-type="right-running-head">
<ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fphys.2024.1392454">10.3389/fphys.2024.1392454</ext-link>
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<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Huang</surname>
<given-names>Xinyu</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
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<contrib contrib-type="author">
<name>
<surname>Jiang</surname>
<given-names>Feng</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
<uri xlink:href="https://loop.frontiersin.org/people/1201273/overview"/>
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<contrib contrib-type="author">
<name>
<surname>Ma</surname>
<given-names>Yongbo</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
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<contrib contrib-type="author">
<name>
<surname>Zhu</surname>
<given-names>Kunpeng</given-names>
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<xref ref-type="aff" rid="aff1">
<sup>1</sup>
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<contrib contrib-type="author">
<name>
<surname>Wang</surname>
<given-names>Zhenyuan</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
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<contrib contrib-type="author">
<name>
<surname>Hua</surname>
<given-names>Zhen</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
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<contrib contrib-type="author" corresp="yes">
<name>
<surname>Yu</surname>
<given-names>Jie</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
<xref ref-type="corresp" rid="c001">&#x2a;</xref>
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<contrib contrib-type="author" corresp="yes">
<name>
<surname>Zhang</surname>
<given-names>Lei</given-names>
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<xref ref-type="aff" rid="aff2">
<sup>2</sup>
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<xref ref-type="corresp" rid="c001">&#x2a;</xref>
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<aff id="aff1">
<sup>1</sup>
<institution>Shandong University of Traditional Chinese Medicine</institution>, <addr-line>Shandon</addr-line>, <country>China</country>
</aff>
<aff id="aff2">
<sup>2</sup>
<institution>Affiliated Hospital of Shandong University of Traditional Chinese Medicine</institution>, <addr-line>Shandon</addr-line>, <country>China</country>
</aff>
<author-notes>
<fn fn-type="edited-by">
<p>
<bold>Edited by:</bold> <ext-link ext-link-type="uri" xlink:href="https://loop.frontiersin.org/people/46616/overview">Robert W. Brock</ext-link>, West Virginia University, United States</p>
</fn>
<fn fn-type="edited-by">
<p>
<bold>Reviewed by:</bold> <ext-link ext-link-type="uri" xlink:href="https://loop.frontiersin.org/people/557407/overview">Dolores Prieto</ext-link>, Universidad Complutense de Madrid, Spain</p>
<p>
<ext-link ext-link-type="uri" xlink:href="https://loop.frontiersin.org/people/1038242/overview">Jiawei Liao</ext-link>, Dalian Medical University, China</p>
</fn>
<corresp id="c001">&#x2a;Correspondence: Jie Yu, <email>Yujie1980learn@126.com</email>; Lei Zhang, <email>zhanglei198222@126.com</email>
</corresp>
</author-notes>
<pub-date pub-type="epub">
<day>11</day>
<month>06</month>
<year>2024</year>
</pub-date>
<pub-date pub-type="collection">
<year>2024</year>
</pub-date>
<volume>15</volume>
<elocation-id>1392454</elocation-id>
<history>
<date date-type="received">
<day>25</day>
<month>03</month>
<year>2024</year>
</date>
<date date-type="accepted">
<day>24</day>
<month>05</month>
<year>2024</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright &#xa9; 2024 Huang, Jiang, Ma, Zhu, Wang, Hua, Yu and Zhang.</copyright-statement>
<copyright-year>2024</copyright-year>
<copyright-holder>Huang, Jiang, Ma, Zhu, Wang, Hua, Yu and Zhang</copyright-holder>
<license xlink:href="http://creativecommons.org/licenses/by/4.0/">
<p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</p>
</license>
</permissions>
<abstract>
<p>The mechanisms underlying the occurrence and development of atherosclerosis (AS) are diverse, among which endoplasmic reticulum stress (ERS) is an important mechanism that should not be overlooked. However, up to now, there has been no bibliometric study on the relationship between ERS and AS. To understand the research progress in ERS and AS, this paper conducted a statistical analysis of publications in this field using bibliometrics. A total of 1,035 records were retrieved from the Web of Science Core Collection. CiteSpace, VOSviewer, and the R package &#x201c;bibliometric&#x201d; were used to analyze the spatiotemporal distribution, countries, authors, institutions, journals, references, and keywords of the literature, and to present the basic information of this field through visualized maps, as well as determine the collaboration relationships among researchers in this field. This field has gradually developed and stabilized over the past 20 years. The current research hotspots in this field mainly include the relationship between ERS and AS-related cells, the mechanisms by which ERS promotes AS, related diseases, and associated cytokines, etc. Vascular calcification, endothelial dysfunction, NLRP3 inflammasome, and heart failure represent the frontier research in this field and are becoming new research hotspots. It is hoped that this study will provide new insights for research and clinical work in the field of ERS and AS.</p>
</abstract>
<kwd-group>
<kwd>endoplasmic reticulum stress</kwd>
<kwd>atherosclerosis</kwd>
<kwd>knowledge-map</kwd>
<kwd>Citespace</kwd>
<kwd>VOSviewer</kwd>
<kwd>bibliometrics</kwd>
</kwd-group>
<custom-meta-wrap>
<custom-meta>
<meta-name>section-at-acceptance</meta-name>
<meta-value>Vascular Physiology</meta-value>
</custom-meta>
</custom-meta-wrap>
</article-meta>
</front>
<body>
<sec id="s1">
<title>1 Introduction</title>
<p>Atherosclerosis (AS) is a chronic inflammatory vascular disease in which lipid or fibrous plaques deposit on the inner lining of arteries, causing narrowing of the affected vessels, blood flow obstruction, and ischemia of related tissues (<xref ref-type="bibr" rid="B39">Libby et al., 2019</xref>). Narrowing of blood vessels coupled with the rupture of unstable plaques can lead to platelet aggregation, thrombosis formation, and acute cardiovascular and cerebrovascular diseases. Cardiovascular disease is the leading cause of death worldwide (<xref ref-type="bibr" rid="B5">Benjamin et al., 2017</xref>), and coronary heart disease is a major component of cardiovascular disease. An epidemiological survey conducted in the United States showed that more than 17 million people died from cardiovascular disease in 2015, accounting for 31% of all deaths worldwide, and an estimated 7.4 million people died from coronary heart disease (<xref ref-type="bibr" rid="B74">Organization, 2011</xref>). Moreover, over 75% of deaths from cardiovascular disease occur in low- and middle-income countries worldwide (<xref ref-type="bibr" rid="B74">Organization, 2011</xref>). The high disability rates associated with cardiovascular disease also impose a heavy economic burden on many developing countries.</p>
<p>The endoplasmic reticulum (ER) is an important organelle in eukaryotic cells that controls protein quality and is responsible for protein synthesis, folding, and transport, as well as participating in calcium storage. Research has shown that ERS is a key factor in the development of AS (<xref ref-type="bibr" rid="B66">Tabas, 2010</xref>). The ER membrane contains three types of transmembrane proteins: activating transcription factor 6 (ATF6), double-stranded RNA-dependent protein kinase R-like ER kinase (PERK), and inositol-requiring enzyme 1 (IRE1) (<xref ref-type="bibr" rid="B57">Ron and Walter, 2007</xref>; <xref ref-type="bibr" rid="B1">Adolph et al., 2012</xref>; <xref ref-type="bibr" rid="B26">Hetz, 2012</xref>). When ERS is enhanced, these sensors can recognize and initiate a series of complex adaptive responses to restore ER homeostasis and function, known as the unfolded protein response (UPR). UPR can provide cellular protection when moderately activated, but if the stress exceeds the compensatory capacity of UPR, such as under oxidative stress, hypoxia, or inflammatory reactions, it can disrupt ER homeostasis, enhance ERS, lead to misfolding and accumulation of unfolded proteins in the lumen, along with disturbances in calcium balance. This can activate inflammatory and apoptotic pathways, resulting in cellular and endothelial dysfunction, accelerating plaque formation, and the progression of AS (<xref ref-type="bibr" rid="B35">Lawrence de Koning et al., 2003</xref>; <xref ref-type="bibr" rid="B77">Yang et al., 2020</xref>). The specific mechanism (shown in <xref ref-type="fig" rid="F1">Figure 1</xref>) involves the separation of the ER membrane-located stress sensors IRE1, PERK, and ATF6 from their protein partner Bip. IRE1 splices XBP1 mRNA to generate spliced XBP1 and recruits apoptosis signal-regulating kinase 1 (ASK1) and TNF receptor-associated factor 2 (TRAF2) (<xref ref-type="bibr" rid="B83">Zhu and Lee, 2015</xref>; <xref ref-type="bibr" rid="B36">Lebeaupin et al., 2018</xref>), leading to the activation of JNK and NF-kB, inducing inflammation and cell apoptosis. Activated PERK phosphorylates the eukaryotic initiation factor 2&#x3b1; (eIF2&#x3b1;), indirectly inhibiting protein synthesis and RNA transcription (<xref ref-type="bibr" rid="B77">Yang et al., 2020</xref>), while enhanced phosphorylated eIF2&#x3b1; promotes ATF4 mRNA translation, upregulating the transcription factor C/EBP homologous protein (CHOP), inducing gene expression involved in autophagy, oxidative stress, and apoptosis (<xref ref-type="bibr" rid="B56">Ren et al., 2021</xref>). Unfolded proteins in the ER lumen activate the JNK and CHOP pathways after the dissociation of ATF6 and heavy chain-binding protein (Bip)/GRP78(11). Under sustained ER stress conditions, the activated CHOP/GADD153, Caspase-12, and JNK pathways participate in inducing cell apoptosis. Additionally, the activation of the TRAF2-mediated NF-&#x3ba;B pathway induces the production of NLRP3 inflammasome (NLRP3) and inflammatory factors such as interleukins, triggering an inflammatory response (<xref ref-type="bibr" rid="B7">Bravo et al., 2011</xref>; <xref ref-type="bibr" rid="B53">Oakes and Papa, 2015</xref>). All of these findings indicate the significant role of ERS in the formation and progression of atherosclerosis.</p>
<fig id="F1" position="float">
<label>FIGURE 1</label>
<caption>
<p>Mechanisms of ERS for AS. This figure illustrates the process by which the three stress sensors, IRE1, PERK, and ATF6, located on the ER membrane, induce inflammation and cell apoptosis through distinct mechanisms.</p>
</caption>
<graphic xlink:href="fphys-15-1392454-g001.tif"/>
</fig>
<p>Bibliometrics emerged in the early 20th century and developed into an independent discipline in 1969. It has been widely applied in literature analysis. Bibliometrics provides quantitative and qualitative methods for investigating published literature in various fields. By analyzing specific information such as authors, countries, institutions, journals, and references of published literature, bibliometrics enables us to obtain information about the development status, distribution patterns, and research hotspots in relevant fields. It has become one of the popular techniques for evaluating the credibility, quality, and impact of academic work (<xref ref-type="bibr" rid="B16">Ellegaard and Wallin, 2015</xref>; <xref ref-type="bibr" rid="B58">Rondanelli et al., 2016</xref>). Quantitative analysis of literature-related data combined with visual presentations can make research results more intuitive. A search of literature related to ERS and AS reveals that although numerous studies are exploring this field from different perspectives, the use of bibliometric methods to analyze the research status in this field is lacking.</p>
</sec>
<sec sec-type="methods" id="s2">
<title>2 Methods</title>
<sec id="s2-1">
<title>2.1 Data collection</title>
<p>Web of Science is a globally trusted and authoritative scientific citation database that covers multiple fields including natural sciences, engineering technology, biomedical sciences, social sciences, arts, and humanities. To ensure the coverage and authority of the data, the Web of Science was selected as the data source, the indexes were selected as SSCI and SCIE, the search strategy selected was TS&#x3d; (&#x201c;endoplasmic reticulum stress&#x201d; OR &#x201c;Endoplasmic Reticulum Stresses&#x201d; OR &#x201c;Reticulum Stress, Endoplasmic&#x201d; OR &#x201c;Reticulum Stresses, Endoplasmic&#x201d; OR &#x201c;Stresses, Endoplasmic Reticulum&#x201d; OR &#x201c;Stress, Endoplasmic Reticulum&#x201d;) AND TS&#x3d; (&#x201c;Atherosclerosis&#x201d; OR &#x201c;Atheroscleroses&#x201d; OR &#x201c;Atherogenesis&#x201d;). To avoid deviations caused by daily data updates, the time span was set from 1 January 2000 to 1 February 2023. A total of 1,048 documents were obtained, and 1,035 documents were finally used in the study. The search results were exported with &#x201c;Plain Text file&#x201d; and the record content chose &#x201c;Full Record and Cited Reference&#x201d;, and stored in download_&#x2a;.txt format. The flowchart was shown in <xref ref-type="fig" rid="F2">Figure 2</xref>.</p>
<fig id="F2" position="float">
<label>FIGURE 2</label>
<caption>
<p>Flowchart illustrating the search strategy and selection process in ERS and AS.</p>
</caption>
<graphic xlink:href="fphys-15-1392454-g002.tif"/>
</fig>
</sec>
<sec id="s2-2">
<title>2.2 Data analysis and visualization</title>
<p>In this study, CiteSpace, VOSviewer and the R package of " bibliometric&#x201d; were applied to collect information on ERS and AS and draw knowledge maps. These software programs have complementary advantages. CiteSpace uses a set-theoretic data standardization method to measure the similarity of knowledge units. Similarity algorithms are used to obtain Timezone and Timeline views within time slices, which clearly outline the evolution of knowledge in this field over time, enabling understanding of the development dynamics and exploration of new research hotspots (<xref ref-type="bibr" rid="B8">Chen, 2006</xref>). VOSviewer uses a probability-based data standardization method and provides multiple visualizations in co-authorship, co-citation, and keyword sections, including Network Visualization, Overlay Visualization, and Density Visualization, with the advantages of simple operation and beautiful images (<xref ref-type="bibr" rid="B73">van Eck and Waltman, 2010</xref>). R language is a programming language and operating environment used for statistical analysis, graphical reports, and reporting. &#x201c;bibliometric&#x201d; is an R language software package developed based on bibliometrics. It uses its powerful computing ability to extract multiple analysis indicators of literature and can achieve visual analysis of bibliometric analysis (<xref ref-type="bibr" rid="B2">Aria et al., 2017</xref>). Firstly, we used visualized maps of annual publications, countries, authors, institutions, and journal publications to intuitively display the basic output of this field. Secondly, based on highly co-cited journals and literature, we presented the knowledge base of this field. Finally, based on co-occurrence graphs of keywords (including keyword clustering, timeline, and highlight maps), we showed changes in research hotspots in this field and identified and discovered new hotspots.</p>
</sec>
</sec>
<sec sec-type="results" id="s3">
<title>3 Results</title>
<sec id="s3-1">
<title>3.1 Temporal distribution map of the literature</title>
<p>From January 2000 to December 2023, a total of 1,035 publications were published in this field. <xref ref-type="fig" rid="F3">Figure 3</xref> shows the trend of literature production in this field over time. The first relevant literature on ERS and AS appeared in 2000, and since then, research on ERS and AS has shown a steady and significant increase. It reached its peak in 2017 with 91 publications. After that, the research intensity on ERS and AS slightly declined but still exhibited a fluctuating upward trend. As the statistics for 2023 are not yet complete, there is a downward trend starting from 2021, and the number of publications in 2023 reached its lowest point at 48.</p>
<fig id="F3" position="float">
<label>FIGURE 3</label>
<caption>
<p>Trends in the growth of publications and the number of cumarticles.</p>
</caption>
<graphic xlink:href="fphys-15-1392454-g003.tif"/>
</fig>
</sec>
<sec id="s3-2">
<title>3.2 Distribution of countries/regions</title>
<p>As shown in <xref ref-type="fig" rid="F4">Figure 4</xref> and <xref ref-type="table" rid="T1">Table 1</xref>, China has the highest number of publications, with a total of 348 papers. The following countries are the United States, Canada, Japan, and South Korea, with 318, 70, 62, and 50 publications respectively, accounting for 33.62%, 30.72%, 6.76%, 5.99%, and 4.83% of the total publication count, surpassing 80% of the total. This suggests that these countries have made significant contributions to the field, while also highlighting the uneven development of research in this domain across different countries/regions. Among the top ten countries in terms of publication count displayed in the table, six countries have a centrality score exceeding 0.1: PEOPLES R CHINA (0.26), United States (0.51), Canada (0.1), ITALY (0.14), ENGLAND (0.27), and FRANCE (0.17). These scores indicate that these six countries hold an important position in research on ERS and AS. It is noteworthy that the United States has the highest citation count, reaching 36,719, followed by China and Canada with 9,528 and 5,052 citations respectively. This highlights the high research value of literature from these countries, which has garnered attention from numerous scholars. VOSviewer parameters were set as follows: Methods (Linlog/modularity) and a minimum number of country documents: 5. The obtained results were retrieved from 62 countries, with 30 meeting the thresholds.</p>
<fig id="F4" position="float">
<label>FIGURE 4</label>
<caption>
<p>Cooperation map of countries/regions in ERS and AS. <bold>(A)</bold> A visual map for VOSviewer network. <bold>(B)</bold> Countries/regions involved in ERS and AS research. The links between countries/regions indicate their collaborations and connections.</p>
</caption>
<graphic xlink:href="fphys-15-1392454-g004.tif"/>
</fig>
<table-wrap id="T1" position="float">
<label>TABLE 1</label>
<caption>
<p>Top 10 most productive countries/regions in ERS and AS.</p>
</caption>
<table>
<thead valign="top">
<tr>
<th align="center">Rank</th>
<th align="center">Countries/Regions</th>
<th align="center">Record count</th>
<th align="center">% of 1,035</th>
<th align="center">Average per Item</th>
<th align="center">Citations</th>
<th align="center">Total link strength</th>
<th align="center">Centrality</th>
</tr>
</thead>
<tbody valign="top">
<tr>
<td align="center">1</td>
<td align="center">PEOPLES R CHINA</td>
<td align="center">348</td>
<td align="center">33.66</td>
<td align="center">27.40</td>
<td align="center">9,528</td>
<td align="center">78</td>
<td align="center">0.26</td>
</tr>
<tr>
<td align="center">2</td>
<td align="center">United States</td>
<td align="center">318</td>
<td align="center">30.72</td>
<td align="center">115.47</td>
<td align="center">36,719</td>
<td align="center">170</td>
<td align="center">0.51</td>
</tr>
<tr>
<td align="center">3</td>
<td align="center">Canada</td>
<td align="center">70</td>
<td align="center">6.76</td>
<td align="center">72.17</td>
<td align="center">5,052</td>
<td align="center">44</td>
<td align="center">0.1</td>
</tr>
<tr>
<td align="center">4</td>
<td align="center">Japan</td>
<td align="center">62</td>
<td align="center">5.99</td>
<td align="center">74.03</td>
<td align="center">4,590</td>
<td align="center">37</td>
<td align="center">0.08</td>
</tr>
<tr>
<td align="center">5</td>
<td align="center">South korea</td>
<td align="center">50</td>
<td align="center">4.83</td>
<td align="center">35.28</td>
<td align="center">1764</td>
<td align="center">15</td>
<td align="center">0.01</td>
</tr>
<tr>
<td align="center">6</td>
<td align="center">Italy</td>
<td align="center">48</td>
<td align="center">4.64</td>
<td align="center">54.21</td>
<td align="center">2,602</td>
<td align="center">28</td>
<td align="center">0.14</td>
</tr>
<tr>
<td align="center">7</td>
<td align="center">Germany</td>
<td align="center">44</td>
<td align="center">4.25</td>
<td align="center">109.5</td>
<td align="center">4,818</td>
<td align="center">54</td>
<td align="center">0.05</td>
</tr>
<tr>
<td align="center">8</td>
<td align="center">England</td>
<td align="center">40</td>
<td align="center">3.86</td>
<td align="center">121.45</td>
<td align="center">4,858</td>
<td align="center">48</td>
<td align="center">0.27</td>
</tr>
<tr>
<td align="center">9</td>
<td align="center">Spain</td>
<td align="center">31</td>
<td align="center">2.99</td>
<td align="center">52.65</td>
<td align="center">1,632</td>
<td align="center">12</td>
<td align="center">0.06</td>
</tr>
<tr>
<td align="center">10</td>
<td align="center">France</td>
<td align="center">27</td>
<td align="center">2.61</td>
<td align="center">75.37</td>
<td align="center">2035</td>
<td align="center">31</td>
<td align="center">0.17</td>
</tr>
</tbody>
</table>
</table-wrap>
<p>According to the analysis of collaborative authors, VOSviewer divided countries into different collaboration clusters, distinguished by different colored nodes. The size of the nodes represents the number of publications, and the thickness of the lines indicates the number of connections between nodes (<xref ref-type="fig" rid="F3">Figure 3A</xref>). <xref ref-type="fig" rid="F3">Figure 3A</xref> shows that countries that collaborate more with the United States include China, Canada, the United Kingdom, Japan, France, Germany, Italy, South Korea, and others. Countries that collaborate more with China include the United States, Canada, the United Kingdom, Turkey, and others. Countries that collaborate more with Canada include China, the United States, the United Kingdom, France, and others. <xref ref-type="fig" rid="F3">Figure 3B</xref> displays a collaboration map of authors in ERS and AS based on their countries/regions. The darker the color, the higher the publication count. The lines represent collaborative relationships between countries, and the line thickness represents the strength of collaboration. Interestingly, the more frequent the contributions between countries, the greater the output, as exemplified by China and the United States, where the figure showed that the lines crossing them are numerous and thick, suggesting that China and the United States play an important role in the development of cooperation in this field. Thus China and the United States are both the countries that produce the most output and work closely with Canada, France, Germany, and Japan.</p>
</sec>
<sec id="s3-3">
<title>3.3 Distribution of authors and research institutions</title>
<p>Analyzing the literature authors allows us to identify the representative scholars and core research forces in this field. According to Price&#x2019;s Law, the minimum publication requirement for core authors in a particular field is given by m &#x3d; 0.749 &#x2a; &#x221a;nmax (where nmax is the maximum number of publications by any author)&#x2248;4.43. Therefore, authors with more than four publications (including 4) were identified as core authors in this field, totaling 127 core authors with a combined publication count of 706 papers, accounting for 68.2% of the total publication count. This meets Price&#x2019;s criterion of reaching 50% of the total, indicating that the ERS and AS fields have formed a relatively stable collaborative community.</p>
<p>As shown in <xref ref-type="table" rid="T2">Table 2</xref>, <xref ref-type="table" rid="T5">5</xref> authors have published more than 10 articles. The author with the highest number of publications is Ira Tabas from Columbia University, with a total of 35 articles and 11,329 citations. The second highest is Geoff H Werstuck from McMaster University, with 22 articles and 1,356 citations. Richard C Austin from Henderson Research Center ranks third with 17 articles and 1,582 citations. Yuanyuan Shi from McMaster University is the fourth with 13 articles and 386 citations. Lastly, Ebru Erbay from Ihsan Dogramaci Bilkent University has published 11 articles with 1,454 citations.</p>
<table-wrap id="T2" position="float">
<label>TABLE 2</label>
<caption>
<p>Top 10 authors in T cell and AS.</p>
</caption>
<table>
<thead valign="top">
<tr>
<th align="center">Rank</th>
<th align="center">Author</th>
<th align="center">Record<break/>Count</th>
<th align="center">% of 1,035</th>
<th align="center">Citations</th>
<th align="center">Average<break/>Per Item</th>
<th align="center">H-index</th>
<th align="center">Affiliations</th>
<th align="center">Total link strength</th>
</tr>
</thead>
<tbody valign="top">
<tr>
<td align="center">1</td>
<td align="center">Tabas, Ira</td>
<td align="center">35</td>
<td align="center">3.38</td>
<td align="center">11,329</td>
<td align="center">323.69</td>
<td align="center">32</td>
<td align="center">Columbia University</td>
<td align="center">68</td>
</tr>
<tr>
<td align="center">2</td>
<td align="center">Werstuck, Geoff H</td>
<td align="center">22</td>
<td align="center">2.13</td>
<td align="center">1,356</td>
<td align="center">61.64</td>
<td align="center">16</td>
<td align="center">McMaster University</td>
<td align="center">64</td>
</tr>
<tr>
<td align="center">3</td>
<td align="center">Austin, Richard C</td>
<td align="center">17</td>
<td align="center">1.64</td>
<td align="center">1,582</td>
<td align="center">93.06</td>
<td align="center">15</td>
<td align="center">Henderson Res Ctr</td>
<td align="center">94</td>
</tr>
<tr>
<td align="center">4</td>
<td align="center">Shi, Yuanyuan</td>
<td align="center">13</td>
<td align="center">1.26</td>
<td align="center">386</td>
<td align="center">29.69</td>
<td align="center">10</td>
<td align="center">McMaster University</td>
<td align="center">30</td>
</tr>
<tr>
<td align="center">5</td>
<td align="center">Erbay, Ebru</td>
<td align="center">11</td>
<td align="center">1.06</td>
<td align="center">1,454</td>
<td align="center">132.18</td>
<td align="center">8</td>
<td align="center">Ihsan Dogramaci Bilkent University</td>
<td align="center">81</td>
</tr>
<tr>
<td align="center">6</td>
<td align="center">Zou, Ming-Hui</td>
<td align="center">9</td>
<td align="center">0.87</td>
<td align="center">929</td>
<td align="center">103.22</td>
<td align="center">8</td>
<td align="center">Georgia State University</td>
<td align="center">30</td>
</tr>
<tr>
<td align="center">7</td>
<td align="center">Bernal-mizrachi, Carlos</td>
<td align="center">8</td>
<td align="center">0.77</td>
<td align="center">872</td>
<td align="center">109</td>
<td align="center">8</td>
<td align="center">Washington University</td>
<td align="center">47</td>
</tr>
<tr>
<td align="center">8</td>
<td align="center">Davies, Peter F</td>
<td align="center">8</td>
<td align="center">0.77</td>
<td align="center">759</td>
<td align="center">94.88</td>
<td align="center">8</td>
<td align="center">University of Pennsylvania</td>
<td align="center">16</td>
</tr>
<tr>
<td align="center">9</td>
<td align="center">Passarelli, Marisa</td>
<td align="center">8</td>
<td align="center">0.77</td>
<td align="center">146</td>
<td align="center">18.25</td>
<td align="center">8</td>
<td align="center">Universidade de Sao Paulo</td>
<td align="center">37</td>
</tr>
<tr>
<td align="center">10</td>
<td align="center">Tall, Alan R</td>
<td align="center">8</td>
<td align="center">0.77</td>
<td align="center">1,046</td>
<td align="center">130.75</td>
<td align="center">8</td>
<td align="center">Columbia University</td>
<td align="center">34</td>
</tr>
</tbody>
</table>
</table-wrap>
<p>VOSviewer parameters were set as follows: Methods (Linlog/modularity) and a minimum number of documents of an author: 3. The obtained results were retrieved for 5,361 authors, and 240 met the thresholds. Based on the analysis of collaborative authors, VOSviewer categorizes authors into 7 clusters. To enhance the visual display, the author co-occurrence network is optimized and presented using Pjake software (<xref ref-type="fig" rid="F5">Figure 5A</xref>). Each node in <xref ref-type="fig" rid="F5">Figure 5A</xref> represents an individual author, where the size of the circle corresponds to the number of publications by each author. The lines between nodes depict the collaborative relationships between authors, with thicker lines indicating stronger collaboration. From the figure, it can be observed that Tabas, Ira has close collaborations with authors such as Tall, Alan R, Seimon, Tracie A, and Fisher, Edward A. Similarly, Erbay, Ebru, Weber, Christian, Mallat, Ziad, and other authors have tight collaborations. Dong, yunzhou, Chen, hong, Cowan, Douglas Bdeng, as well as Zou, Minhui, Xie, Zhonglin, Zhang, Miao, and others also exhibit strong collaborative relationships. <xref ref-type="fig" rid="F5">Figure 5A</xref> clearly demonstrates the clustering of the seven authors, with dense connections within each cluster and relatively sparse and thinner connections between different clusters. This suggests that authors have formed stable collaborative networks, with fewer authors breaking existing collaborations to seek new partners. CiteSpace parameters were set as follows: time slice (2000&#x2013;2023), year per slice (<xref ref-type="bibr" rid="B5">Benjamin et al., 2017</xref>), term source(entire selection), node type(author), and selection criteria (top N &#x3d; 50). Other parameters were left at the default settings. <xref ref-type="fig" rid="F4">Figure 4B</xref> shows the visual map of authors for CiteSpace network. The size of nodes represents the number of outputs of authors, and different colors represent different years. From 2000 to 2023, the color changes from purple to red.</p>
<fig id="F5" position="float">
<label>FIGURE 5</label>
<caption>
<p>A collaborative network display between authors and institutions from ERS and AS. <bold>(A)</bold> A visual map for the VOSviewer network among authors. <bold>(B)</bold> A visual map for the CiteSpace network among authors. <bold>(C)</bold> A visual map for the VOSviewer network among institutions. <bold>(D)</bold> A visual map for the CiteSpace network among institutions.</p>
</caption>
<graphic xlink:href="fphys-15-1392454-g005.tif"/>
</fig>
<p>Based on the data in <xref ref-type="table" rid="T2">Table 2</xref> and the author&#x2019;s co-occurrence maps presented by VOSviewer and CiteSpace, it is evident that Tabas, Ira is an absolute core research force in the field of ERS and AS. Authors such as Werstuck, Geoff H and Austin, Richard C have also made significant contributions to research in this field.</p>
<p>As shown in <xref ref-type="fig" rid="F5">Figure 5</xref> and <xref ref-type="table" rid="T3">Table 3</xref>, Columbia University is the institution with the highest number of publications (<xref ref-type="bibr" rid="B4">Battson et al., 2017</xref>), followed by McMaster University (<xref ref-type="bibr" rid="B49">Milutinovi&#x107; et al., 2020</xref>), University of California System (<xref ref-type="bibr" rid="B19">Esse et al., 2019</xref>), Harvard University (<xref ref-type="bibr" rid="B30">Ji et al., 2021</xref>), and Capital Medical University (<xref ref-type="bibr" rid="B67">Tabas and Ron, 2011</xref>). The top five institutions in terms of citation count are Columbia University (13,154), New York University (3,751), University of California System (3,208), University of Washington (3,205), and Harvard University (2,951).</p>
<table-wrap id="T3" position="float">
<label>TABLE 3</label>
<caption>
<p>Top 5 institutions based on publications (Rank a) and citations (Rank b).</p>
</caption>
<table>
<thead valign="top">
<tr>
<th align="center">Rank</th>
<th align="center">organization</th>
<th align="center">Documents</th>
<th align="center">Citations</th>
<th align="center">Total link strength</th>
<th align="center">Centrality</th>
</tr>
</thead>
<tbody valign="top">
<tr>
<td align="center">1a</td>
<td align="center">Columbia University</td>
<td align="center">42</td>
<td align="center">13,154</td>
<td align="center">27</td>
<td align="center">0.1</td>
</tr>
<tr>
<td align="center">2a</td>
<td align="center">McMaster University</td>
<td align="center">39</td>
<td align="center">2,441</td>
<td align="center">25</td>
<td align="center">0.07</td>
</tr>
<tr>
<td align="center">3a</td>
<td align="center">University of California System</td>
<td align="center">37</td>
<td align="center">3,208</td>
<td align="center">33</td>
<td align="center">0.07</td>
</tr>
<tr>
<td align="center">4a</td>
<td align="center">Harvard University</td>
<td align="center">33</td>
<td align="center">2,951</td>
<td align="center">26</td>
<td align="center">0.09</td>
</tr>
<tr>
<td align="center">5a</td>
<td align="center">Capital Medical University</td>
<td align="center">26</td>
<td align="center">511</td>
<td align="center">16</td>
<td align="center">0.03</td>
</tr>
<tr>
<td align="center">1b</td>
<td align="center">Columbia University</td>
<td align="center">42</td>
<td align="center">13,154</td>
<td align="center">27</td>
<td align="center">0.1</td>
</tr>
<tr>
<td align="center">2b</td>
<td align="center">New York University</td>
<td align="center">15</td>
<td align="center">3,751</td>
<td align="center">23</td>
<td align="center">0.19</td>
</tr>
<tr>
<td align="center">3b</td>
<td align="center">University of California System</td>
<td align="center">37</td>
<td align="center">3,208</td>
<td align="center">33</td>
<td align="center">0.07</td>
</tr>
<tr>
<td align="center">4b</td>
<td align="center">University of Washington</td>
<td align="center">16</td>
<td align="center">3,205</td>
<td align="center">29</td>
<td align="center">0.03</td>
</tr>
<tr>
<td align="center">5b</td>
<td align="center">Harvard University</td>
<td align="center">33</td>
<td align="center">2,951</td>
<td align="center">26</td>
<td align="center">0.09</td>
</tr>
</tbody>
</table>
</table-wrap>
<p>The VOSviewer was set as follows: the minimum number of institutions was 5. Of the 1,192 organizations, 96 met the thresholds. By utilizing Pjake software, the clustering of institutions was visualized and presented in <xref ref-type="fig" rid="F5">Figure 5C</xref>. The institutions were divided into 11 clusters. The first cluster includes Boston University, Chongqing Medical University, Fudan University, INSERM, Guangzhou Medical University, Nanchang University, and others. The second cluster includes China Pharmaceutical University, Chinese People&#x2019;s Liberation Army General Hospital, Huazhong University of Science and Technology, Shandong University, Wuhan University, and so on. The third cluster includes Capital Medical University, Chinese Academy of Sciences, China Academy of Chinese Medical Sciences, Nanjing Medical University, and so on. The forth cluster includes the Chinese University of Hong Kong, Dalian Medical University, Harbin Medical University, Monash University and so on. The fifth cluster includes Cleveland Clinic Foundation, McMaster University, University of Iowa, and so on. The sixth cluster includes Baylor College of Medicine, Johns Hopkins University, National Taiwan University, University of Michigan and so on. The seventh cluster includes University of Tokyo, Xian Jiaotong University, King&#x2019;s College London, Queen Mary University London and so on. The eighth cluster includes Columbia University, New York University, Yale University, and so on. The ninth clusters includes Harvard Medical School, Harvard University, University of Toledo and so on. The 10th cluster includes University of California System, University of Pennsylvania, University of Toronto and so on. The 11th cluster includes University of Washington, Emory University, Temple University, and so on. The CiteSpace parameters were set as follows: time slicing (2000&#x2013;2023), year per slice(1), term source is all, and other parameters were set to default values. <xref ref-type="fig" rid="F4">Figure 4D</xref> displays the visual map of the results. Nodes representing Columbia University, McMaster University, and the University of California System are relatively larger, indicating significant contributions of these institutions in the ERS and AS fields. In <xref ref-type="fig" rid="F5">Figure 5C,D</xref>, all nodes are interconnected closely, suggesting extensive collaborations among different institutions.</p>
</sec>
<sec id="s3-4">
<title>3.4 Distribution of journals</title>
<p>A total of 1,035 articles were published in 373 journals. <xref ref-type="fig" rid="F6">Figure 6</xref> and <xref ref-type="table" rid="T4">Table 4</xref> present the top ten journals with the highest number of publications, along with their JCR zones and impact factors. Arteriosclerosis Thrombosis and Vascular Biology published the highest number of articles in the ERS and AS fields (31.3%), followed by the Journal of Biological Chemistry (29, 2.8%), International Journal of Molecular Sciences (27, 2.61%), Circulation Research (23, 2.22%), and Atherosclerosis (21, 2.03%). Circulation had the highest IF of 37.8. Among the top 10 journals, 7 (Arteriosclerosis Thrombosis and Vascular Biology, International Journal of Molecular sciences, Circulation Research, Antioxidants &#x26; Redox Signaling, Frontiers in Pharmacology, Cardiovascular research and Circulation) journals are all located in the Q1 JCR division, and their IF exceed 5. <xref ref-type="fig" rid="F6">Figure 6A</xref> illustrates the publication volume of the top 10 journals, while <xref ref-type="fig" rid="F6">Figure 6B</xref> displays the temporal trend of publication volume for these journals. It can be observed from the figures that the publication volume of each journal has been increasing over the years, particularly since 2010, when there has been a significant surge in the number of publications.</p>
<fig id="F6" position="float">
<label>FIGURE 6</label>
<caption>
<p>Showcase of issuing journals. <bold>(A)</bold>Top 10 journals in terms of number of publications. <bold>(B)</bold> Trends in the number of articles published in the top ten journals over time.</p>
</caption>
<graphic xlink:href="fphys-15-1392454-g006.tif"/>
</fig>
<table-wrap id="T4" position="float">
<label>TABLE 4</label>
<caption>
<p>The top 10 journals in ERS and AS.</p>
</caption>
<table>
<thead valign="top">
<tr>
<th align="center">Rank</th>
<th align="center">Sources</th>
<th align="center">N(%)</th>
<th align="center">IF<xref ref-type="table-fn" rid="Tfn1">
<sup>a</sup>
</xref>(2022)</th>
<th align="center">JCR<xref ref-type="table-fn" rid="Tfn2">
<sup>b</sup>
</xref> (2022)</th>
</tr>
</thead>
<tbody valign="top">
<tr>
<td align="center">1</td>
<td align="center">ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY</td>
<td align="center">31(3.00)</td>
<td align="center">8.700</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">2</td>
<td align="center">JOURNAL OF BIOLOGICAL CHEMISTRY</td>
<td align="center">29(2.80)</td>
<td align="center">4.800</td>
<td align="center">Q2</td>
</tr>
<tr>
<td align="center">3</td>
<td align="center">INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES</td>
<td align="center">27(2.61)</td>
<td align="center">5.600</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">4</td>
<td align="center">CIRCULATION RESEARCH</td>
<td align="center">23(2.22)</td>
<td align="center">20.100</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">5</td>
<td align="center">ATHEROSCLEROSIS</td>
<td align="center">21(2.03)</td>
<td align="center">5.300</td>
<td align="center">Q2</td>
</tr>
<tr>
<td align="center">6</td>
<td align="center">ANTIOXIDANTS &#x26; REDOX SIGNALING</td>
<td align="center">19(1.84)</td>
<td align="center">6.600</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">7</td>
<td align="center">PLOS ONE</td>
<td align="center">19(1.84)</td>
<td align="center">3.700</td>
<td align="center">Q2</td>
</tr>
<tr>
<td align="center">8</td>
<td align="center">FRONTIERS IN PHARMACOLOGY</td>
<td align="center">17(1.64)</td>
<td align="center">5.600</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">9</td>
<td align="center">CARDIOVASCULAR RESEARCH</td>
<td align="center">16(1.55)</td>
<td align="center">10.800</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">10</td>
<td align="center">CIRCULATION</td>
<td align="center">16(1.55)</td>
<td align="center">37.800</td>
<td align="center">Q1</td>
</tr>
</tbody>
</table>
<table-wrap-foot>
<fn id="Tfn1">
<label>
<sup>a</sup>
</label>
<p>IF: impact factor.</p>
</fn>
<fn id="Tfn2">
<label>
<sup>b</sup>
</label>
<p>JCR: journal citation reports.</p>
</fn>
</table-wrap-foot>
</table-wrap>
<p>
<xref ref-type="table" rid="T5">Table 5</xref> presents the top 10 most cited journals, with seven of them ranked in Q1 of JCR. The highest impact factor journal is Nature (64.8), while the top three most cited journals are the Journal of Biological Chemistry (4,011 citations), Arteriosclerosis Thrombosis and Vascular Biology (3,196 citations), and Circulation (2,881 citations), all outstanding journals in JCR zones one and 2. The VOSviewer was set to display a minimum of 200 institutions, with 70 sources meeting the thresholds. <xref ref-type="fig" rid="F7">Figure 7</xref> shows that the co-citation network of journals is composed of four clusters, corresponding to the four colors in the figure. In the first and second clusters, the research is related to medicine and biochemistry. The first cluster focuses on the microbial level of research, such as cells, while the second cluster is more related to cardiovascular diseases. The third cluster is associated with inflammation and immunity, and the fourth cluster consists of only one review medical journal. The main purpose of citing these clustered journals is to analyze and review existing research, providing theoretical and empirical support for future studies. Among them, the results of the second and third clusters indicate that in the fields of ERS (Environmental and Resources Science) and AS (Aerosol Science), more scholars focus on cardiovascular diseases within the circulatory system. The research hotspot lies in the investigation of inflammatory and immune mechanisms.</p>
<table-wrap id="T5" position="float">
<label>TABLE 5</label>
<caption>
<p>Top 10 co-cited journals in T cell and AS.</p>
</caption>
<table>
<thead valign="top">
<tr>
<th align="center">Rank</th>
<th align="center">Sources</th>
<th align="center">Frequency</th>
<th align="center">IF<xref ref-type="table-fn" rid="Tfn3">
<sup>a</sup>
</xref>(2022)</th>
<th align="center">JCR<xref ref-type="table-fn" rid="Tfn4">
<sup>b</sup>
</xref> (2022)</th>
</tr>
</thead>
<tbody valign="top">
<tr>
<td align="center">1</td>
<td align="center">Journal Of Biological Chemistry</td>
<td align="center">4,011</td>
<td align="center">4.8</td>
<td align="center">Q2</td>
</tr>
<tr>
<td align="center">2</td>
<td align="center">Arteriosclerosis Thrombosis And Vascular Biology</td>
<td align="center">3,196</td>
<td align="center">8.7</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">3</td>
<td align="center">Circulation</td>
<td align="center">2,881</td>
<td align="center">37.8</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">4</td>
<td align="center">Circulation Research</td>
<td align="center">2,604</td>
<td align="center">20.1</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">5</td>
<td align="center">Journal Of Clinical Investigation</td>
<td align="center">2,101</td>
<td align="center">15.9</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">6</td>
<td align="center">Proceedings of The National Academy Of Sciences of The United States</td>
<td align="center">1987</td>
<td align="center">11.1</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">7</td>
<td align="center">Nature</td>
<td align="center">1,676</td>
<td align="center">64.8</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">8</td>
<td align="center">Diabetes</td>
<td align="center">1,509</td>
<td align="center">7.7</td>
<td align="center">Q1</td>
</tr>
<tr>
<td align="center">9</td>
<td align="center">Atherosclerosis</td>
<td align="center">1,332</td>
<td align="center">5.3</td>
<td align="center">Q2</td>
</tr>
<tr>
<td align="center">10</td>
<td align="center">Plos One</td>
<td align="center">1,221</td>
<td align="center">3.7</td>
<td align="center">Q2</td>
</tr>
</tbody>
</table>
<table-wrap-foot>
<fn id="Tfn3">
<label>
<sup>a</sup>
</label>
<p>IF: impact factor.</p>
</fn>
<fn id="Tfn4">
<label>
<sup>b</sup>
</label>
<p>JCR: journal citation reports.</p>
</fn>
</table-wrap-foot>
</table-wrap>
<fig id="F7" position="float">
<label>FIGURE 7</label>
<caption>
<p>Visualization of co-cited journals. According to the journal content, four clusters&#x2014;red, green, blue, and yellow&#x2014;are presented, with the red cluster comprising the most journals and being the largest cluster.</p>
</caption>
<graphic xlink:href="fphys-15-1392454-g007.tif"/>
</fig>
</sec>
<sec id="s3-5">
<title>3.5 Co-cited reference and reference burst</title>
<p>Co-citation refers to the frequency at which two documents are both cited by another document. The table displays the top ten most cited articles. The most frequently cited article is &#x201c;The Role of Endoplasmic Reticulum Stress in the Progression of Atherosclerosis&#x201d; by Ira Tabas, published in Circulation Research (66 citations) (<xref ref-type="bibr" rid="B66">Tabas, 2010</xref>). The second one is &#x201c;Reduced Apoptosis and Plaque Necrosis in Advanced Atherosclerotic Lesions of Apoe/and Ldlr/Mice Lacking CHOP&#x201d; by Edward Thorp, published in Cell Metabolism (58 citations) (<xref ref-type="bibr" rid="B70">Thorp et al., 2009</xref>). The third one includes two articles: &#x201c;Reducing endoplasmic reticulum stress through a macrophage lipid chaperone alleviates atherosclerosis&#x201d; by Ebru Erbay, published in Nature Medicine (57 citations) (<xref ref-type="bibr" rid="B18">Erbay et al., 2009</xref>), and &#x201c;Increased Endoplasmic Reticulum Stress in Atherosclerotic Plaques Associated With Acute Coronary Syndrome&#x201d; by Masafumi Myoishi, MD, published in Coronary Heart Disease (57 citations) (<xref ref-type="bibr" rid="B51">Myoishi et al., 2007</xref>). Among the top ten cited articles, five are review articles and five are experimental articles. Based on the co-citation map of literature (<xref ref-type="fig" rid="F8">Figure 8A</xref>), co-citation literature emergence detection was performed, and <xref ref-type="fig" rid="F8">Figure 8B</xref> shows the top 20 most prominent reference literature. The blue line represents the timeline, and the red part on the blue timeline represents the start year, end year, and duration of emergence. The strongest emerging reference literature is &#x201c;The Role of Endoplasmic Reticulum Stress in the Progression of Atherosclerosis&#x201d; published in 2010, with an intensity of 22.76. These articles are outstanding contributions in the ERS and AS fields. Among them, &#x201c;The Role of Endoplasmic Reticulum Stress in the Progression of Atherosclerosis&#x201d; discusses the role and treatment strategies of endoplasmic reticulum stress in mediating cell apoptosis and inflammatory responses in endothelial cells, smooth muscle cells, and macrophages in atherosclerosis (<xref ref-type="bibr" rid="B66">Tabas, 2010</xref>). The high citation and high intensity of emergence both indicate the important influence of this review article.</p>
<fig id="F8" position="float">
<label>FIGURE 8</label>
<caption>
<p>
<bold>(A)</bold> References co-citation network in ERS and AS. <bold>(B)</bold> Top 20 references with the strongest citation bursts in ERS and AS.</p>
</caption>
<graphic xlink:href="fphys-15-1392454-g008.tif"/>
</fig>
</sec>
<sec id="s3-6">
<title>3.6 Research hotspots and frontier analysis</title>
<p>Keywords are important vocabulary that can summarize the main content of a document. The frequency of keywords reflects the changing trends of research in different periods. Visual analysis of keywords provides an intuitive understanding of the research trends in the ERS and AS fields, which helps track the development dynamics of the ERS and AS research areas.</p>
<p>As displayed in <xref ref-type="table" rid="T6">Table 6</xref>, in addition to endoplasmic reticulum stress(887) and atherosclerosis(586), keywords with higher frequency in this study include apoptosis(254), oxidative stress(248), unfolded protein response(223), inflammation(200), vascular endothelial cell(180), cardiovascular disease(174), activation(160), smooth muscle cells(150). Among these keywords, expression, nf-kappa b, macrophage, insulin resistance, and ldl appeared more than 100 times, indicating that they are the focus of the research.</p>
<table-wrap id="T6" position="float">
<label>TABLE 6</label>
<caption>
<p>Top 20 keywords in ERS and AS.</p>
</caption>
<table>
<thead valign="top">
<tr>
<th align="center">Rank</th>
<th align="center">Keyword</th>
<th align="center">occurrences</th>
<th align="center">Total link strength</th>
<th align="center">Rank</th>
<th align="center">Keyword</th>
<th align="center">occurrence</th>
<th align="center">Total link strength</th>
</tr>
</thead>
<tbody valign="top">
<tr>
<td align="center">1</td>
<td align="center">endoplasmic reticulum stress</td>
<td align="center">887</td>
<td align="center">5,593</td>
<td align="center">11</td>
<td align="center">expression</td>
<td align="center">132</td>
<td align="center">884</td>
</tr>
<tr>
<td align="center">2</td>
<td align="center">atherosclerosis</td>
<td align="center">586</td>
<td align="center">4,010</td>
<td align="center">12</td>
<td align="center">nf-kappa b</td>
<td align="center">130</td>
<td align="center">917</td>
</tr>
<tr>
<td align="center">3</td>
<td align="center">apoptosis</td>
<td align="center">254</td>
<td align="center">1779</td>
<td align="center">13</td>
<td align="center">macrophage</td>
<td align="center">129</td>
<td align="center">914</td>
</tr>
<tr>
<td align="center">4</td>
<td align="center">oxidative stress</td>
<td align="center">248</td>
<td align="center">1,682</td>
<td align="center">14</td>
<td align="center">insulin resistance</td>
<td align="center">128</td>
<td align="center">914</td>
</tr>
<tr>
<td align="center">5</td>
<td align="center">unfolded protein response</td>
<td align="center">223</td>
<td align="center">1,521</td>
<td align="center">15</td>
<td align="center">ldl</td>
<td align="center">105</td>
<td align="center">720</td>
</tr>
<tr>
<td align="center">6</td>
<td align="center">inflammation</td>
<td align="center">200</td>
<td align="center">1,410</td>
<td align="center">16</td>
<td align="center">diabetes mellitus</td>
<td align="center">89</td>
<td align="center">649</td>
</tr>
<tr>
<td align="center">7</td>
<td align="center">vascular endothelial cell</td>
<td align="center">180</td>
<td align="center">1,347</td>
<td align="center">17</td>
<td align="center">signaling pathway</td>
<td align="center">83</td>
<td align="center">601</td>
</tr>
<tr>
<td align="center">8</td>
<td align="center">cardiovascular disease</td>
<td align="center">174</td>
<td align="center">1,188</td>
<td align="center">18</td>
<td align="center">cholesterol</td>
<td align="center">74</td>
<td align="center">533</td>
</tr>
<tr>
<td align="center">9</td>
<td align="center">activation</td>
<td align="center">160</td>
<td align="center">1,153</td>
<td align="center">19</td>
<td align="center">mice</td>
<td align="center">74</td>
<td align="center">512</td>
</tr>
<tr>
<td align="center">10</td>
<td align="center">smooth muscle cells</td>
<td align="center">150</td>
<td align="center">1,075</td>
<td align="center">20</td>
<td align="center">gene expression</td>
<td align="center">72</td>
<td align="center">476</td>
</tr>
</tbody>
</table>
</table-wrap>
<p>CiteSpace parameters were set as follows: time slice (2000&#x2013;2023), year per slice (<xref ref-type="bibr" rid="B5">Benjamin et al., 2017</xref>), term source(entire selection), node type(author), and selection criteria (top N &#x3d; 50). Other parameters were left at the default settings. The larger the nodes in the graph, the higher the frequency of occurrence of the corresponding keywords. A larger node centrality also indicates the importance of the keyword. The redder the node color, the newer the keyword. Thicker lines between nodes indicate a closer relationship between them. Based on the co-occurrence graph of keywords, we generated keyword clustering graphs, keyword timeline graphs, and the top 25 keywords with the highest prominence intensity (<xref ref-type="fig" rid="F9">Figure 9</xref>).</p>
<fig id="F9" position="float">
<label>FIGURE 9</label>
<caption>
<p>
<bold>(A)</bold> Keywords network in ERS and AS. <bold>(B)</bold> Timeline viewer related to ERS and AS. <bold>(C)</bold> Top 25 keywords with the strongest citation bursts. <bold>(D)</bold> The cluster of keywords in the studies of ERS and AS.</p>
</caption>
<graphic xlink:href="fphys-15-1392454-g009.tif"/>
</fig>
<p>The timeline graph displays the dynamic evolution path of research hotspots represented by keywords. It explores the evolution process of research hotspots in different periods and helps scholars track current and potential hotspots. <xref ref-type="fig" rid="F9">Figure 9B</xref> visually shows the phased research hotspots and development trends in the ERS and AS fields from a temporal perspective. Multiple clusters are formed, labeled as &#x23;0, &#x23;1, &#x23;2, etc. <xref ref-type="fig" rid="F9">Figure 9B</xref> presents 10 clusters, namely, oxidative stress, cholesterol efflux, insulin resistance, express, endothelial cell, endothelial dysfunction, vitamin D, cell death, unfolded protein response, and cystathionine beta-synthase.</p>
<p>The keyword burst graph intuitively displays the phased changes in research hotspots over time. As shown in <xref ref-type="fig" rid="F9">Figure 9C</xref>, the research hotspots from 2000 to 2010 include vascular endothelial cells, risk factors, nitric oxide, plasma homocysteine, and cystathionine beta-synthase, among others. The hotspots from 2017 to 2023 include cardiovascular disease, lipid metabolism, inhibition, nlrp3 inflammasome, and ischemia reperfusion injury, among others. These keywords are also in the period of research outbreak and their popularity shows no sign of decline over time.</p>
<p>Keyword clustering is a classification based on the degree of association between keywords. In CiteSpace software, the likelihood ratio (LLR) is used to create keyword clustering graphs, where a higher number of clustered nodes indicates a higher research hotspot and a smaller cluster index. The modularity value (Q) and average silhouette value (S) are two metrics used to evaluate the clustering effectiveness of CiteSpace. A Q value greater than 0.3 indicates a significant community structure, while an S value above 0.5 suggests reasonable clustering. When the S value reaches 0.7, it is considered to have high clustering efficiency and is convincing (<xref ref-type="bibr" rid="B81">Yue et al., 2015</xref>).</p>
<p>This study formed 10 clusters (Q &#x3d; 0.5427, S &#x3d; 0.7818) with convincing clustering results (shown in <xref ref-type="table" rid="T7">Table 7</xref>). The cluster labels are endothelial dysfunction, inflammation, insulin resistance, unfolded protein response, fatty liver disease, smooth muscle cells, metabolic syndrome, induced apoptosis, scavenger receptor, and cholesterol-loaded macrophages. Clusters &#x23;0, &#x23;6, and &#x23;9 mainly involve the pro-AS effects of ERS on different cells. Clusters &#x23;1, &#x23;2, &#x23;3, &#x23;7, and &#x23;8 mainly involve the specific mechanism by which ERS promotes AS. Clusters &#x23;4 and &#x23;6 are related to diseases associated with ERS and AS.</p>
<table-wrap id="T7" position="float">
<label>TABLE 7</label>
<caption>
<p>Ten keyword clusters.</p>
</caption>
<table>
<thead valign="top">
<tr>
<th align="center">Cluster groups</th>
<th align="center">Key words</th>
</tr>
</thead>
<tbody valign="top">
<tr>
<td align="center">&#x23;0 endothelial dysfunction</td>
<td align="center">endothelial dysfunction, nitric oxide, shear stress, hydrogen sulfide, endothelial growth factor, plasma homocysteine, monocyte chemoattractant protein 1, transcription factor xbp1, vascular remodeling</td>
</tr>
<tr>
<td align="center">&#x23;1 inflammation</td>
<td align="center">Inflammation, macrophages, TNF-&#x3b1;, T cells, AMPK, nlrp3 inflammasome</td>
</tr>
<tr>
<td align="center">&#x23;2 insulin resistance</td>
<td align="center">insulin resistance, type 2 diabetes mellitus, lipid metabolism, protein kinase c, oxidative stress</td>
</tr>
<tr>
<td align="center">&#x23;3 unfolded protein response</td>
<td align="center">unfolded protein response, NF kappa B, c/ebp homologous protein, free cholesterol, macrophage apoptosis, foam cells, vulnerable plaque, bcl-2 genes, ATF4</td>
</tr>
<tr>
<td align="center">&#x23;4 fatty liver disease</td>
<td align="center">fatty liver disease, high density lipoprotein, diet induced obesity, ubiquitin proteasome system, familial hypercholesterolemia, cholesterol oxidation products</td>
</tr>
<tr>
<td align="center">&#x23;5 smooth muscle cells</td>
<td align="center">smooth muscle cells, programmed cell death, glutathione peroxidase</td>
</tr>
<tr>
<td align="center">&#x23;6 metabolic syndrome</td>
<td align="center">metabolic syndrome, ischemia reperfusion injury, alzheimers disease, heart failure, nonalcoholic steatohepatitis</td>
</tr>
<tr>
<td align="center">&#x23;7 induced apoptosis</td>
<td align="center">induced apoptosis, macrophage polarization, PPAR-&#x3b3;, transcription factor foxo1, liver x receptor, ldl oxidation, carboxy terminal hydrolase</td>
</tr>
<tr>
<td align="center">&#x23;8 scavenger receptor</td>
<td align="center">scavenger receptor, adhesion molecules, phagocytosis, necrosis, kinase 3 beta, c reactive protein, palmitic acid</td>
</tr>
<tr>
<td align="center">&#x23;9 cholesterol loaded macrophages</td>
<td align="center">cholesterol loaded macrophages, lipid peroxidation, 9 oxononanoyl cholesterol, apoptosis susceptibility, serum paraoxonase, biological activity</td>
</tr>
</tbody>
</table>
</table-wrap>
</sec>
</sec>
<sec sec-type="discussion" id="s4">
<title>4 Discussion</title>
<sec id="s4-1">
<title>4.1 General information of main findings</title>
<p>This research conducted bibliometric analysis on 1,035 documents from the core collection of the Web of Science database, spanning from 1 January 2000, to 1 December 2023. Utilizing software such as Citespace, Vosviewer, and the R package &#x201c;bibliometric&#x201d;, the study aimed to visually analyze publications, countries, institutions, journals, and co-cited literature in the fields of ERS and AS. The findings revealed a consistent increase in literature publications in the ERS and AS over the initial decade from 2000 to 2013, followed by a fluctuating upward trend, indicating sustained scholarly attention to the field. The United States and China emerged as principal research countries, with literature from countries like the United Kingdom, the United States, Germany, and France exhibiting a high citation rate, signifying the quality and maturity of research in the field.</p>
<p>In terms of authors and journals, specific individuals such as Ira Tabas from Columbia University and certain journals like Circulation demonstrated significant impact and importance in the field. These results delineate the trajectory of research development in the ERS and AS, highlighting research hotspots and emerging frontiers. They assist scholars in selecting appropriate publication outlets and collaborators while providing theoretical underpinnings for future investigations in the field.</p>
</sec>
<sec id="s4-2">
<title>4.2 Knowledge base of ERS and AS</title>
<p>Co-citation refers to two articles being cited by another article at the same time. Highly co-cited research is usually considered the foundation of a field (<xref ref-type="bibr" rid="B40">Lijun et al., 2019</xref>). <xref ref-type="table" rid="T8">Table 8</xref> shows the top ten highly cited articles, including five reviews and five experimental articles. These ten articles explore the relationship between ERS and AS from different perspectives.</p>
<table-wrap id="T8" position="float">
<label>TABLE 8</label>
<caption>
<p>Top 10 cited references of publications in ERS and AS.</p>
</caption>
<table>
<thead valign="top">
<tr>
<th align="center">Rank</th>
<th align="center">Author</th>
<th align="center">Title</th>
<th align="center">Journal</th>
<th align="center">Co-citation</th>
<th align="center">Centrality</th>
</tr>
</thead>
<tbody valign="top">
<tr>
<td align="center">1</td>
<td align="center">Ira Tabas</td>
<td align="center">The Role of Endoplasmic Reticulum Stress in the Progression of Atherosclerosis</td>
<td align="center">Circulation Research</td>
<td align="center">66</td>
<td align="center">0.01</td>
</tr>
<tr>
<td align="center">2</td>
<td align="center">Edward Thorp</td>
<td align="center">Reduced Apoptosis and Plaque Necrosis in Advanced Atherosclerotic Lesions of Apoe/and Ldlr/Mice Lacking CHOP</td>
<td align="center">Cell Metabolism</td>
<td align="center">58</td>
<td align="center">0.07</td>
</tr>
<tr>
<td align="center">3</td>
<td align="center">Ebru Erbay</td>
<td align="center">Reducing endoplasmic reticulum stress through a macrophage lipid chaperone alleviates atherosclerosis</td>
<td align="center">Nature Medicine</td>
<td align="center">57</td>
<td align="center">0.02</td>
</tr>
<tr>
<td align="center">4</td>
<td align="center">Masafumi Myoishi, MD</td>
<td align="center">Increased Endoplasmic Reticulum Stress in Atherosclerotic Plaques Associated With Acute Coronary Syndrome</td>
<td align="center">Coronary Heart Disease</td>
<td align="center">57</td>
<td align="center">0.05</td>
</tr>
<tr>
<td align="center">5</td>
<td align="center">Hotamisligil GS</td>
<td align="center">Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease</td>
<td align="center">Cell</td>
<td align="center">40</td>
<td align="center">0.02</td>
</tr>
<tr>
<td align="center">6</td>
<td align="center">Ira Tabas</td>
<td align="center">Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress</td>
<td align="center">Review</td>
<td align="center">37</td>
<td align="center">0.15</td>
</tr>
<tr>
<td align="center">7</td>
<td align="center">David Ron</td>
<td align="center">Signal integration in the endoplasmic reticulum unfolded protein response</td>
<td align="center">REVIEWS</td>
<td align="center">36</td>
<td align="center">0.03</td>
</tr>
<tr>
<td align="center">8</td>
<td align="center">Hotamisligil GS</td>
<td align="center">Endoplasmic reticulum stress and atherosclerosis</td>
<td align="center">COMMENTARY</td>
<td align="center">36</td>
<td align="center">0</td>
</tr>
<tr>
<td align="center">9</td>
<td align="center">Mete Civelek</td>
<td align="center">Chronic Endoplasmic Reticulum Stress Activates Unfolded Protein Response in Arterial Endothelium in Regions of Susceptibility to Atherosclerosis</td>
<td align="center">Circulation Research</td>
<td align="center">33</td>
<td align="center">0.02</td>
</tr>
<tr>
<td align="center">10</td>
<td align="center">Tracie DeVries-Seimon</td>
<td align="center">Cholesterol-induced macrophage apoptosis requires ER stress pathways and engagement of the type A scavenger receptor</td>
<td align="center">The Journal Of Cell Biology</td>
<td align="center">31</td>
<td align="center">0.16</td>
</tr>
</tbody>
</table>
</table-wrap>
<p>A review published by Ira Tabas in the journal Circulation in 2010 systematically discusses the role of endoplasmic reticulum stress (ERS) in the development of atherosclerosis. This article summarizes that under stimuli such as oxidative stress, oxidized sterols, elevated intracellular cholesterol levels, and saturated fatty acids, the unfolded protein response (UPR) can be prolonged and activated. It provides ample evidence to demonstrate the chronic activation of UPR in atherosclerotic lesion cells, such as endothelial cells, smooth muscle cells, and macrophages. The long-term activation of ERS is believed to influence the formation and vulnerability of atherosclerotic plaques by recruiting inflammatory factors, inducing inflammatory responses, and activating multiple pro-apoptotic signaling pathways (<xref ref-type="bibr" rid="B66">Tabas, 2010</xref>).</p>
<p>The team led by Edward Thorp discovered through experiments that CHOP expression increases in advanced atherosclerotic lesions. By comparing the size and morphology of aortic root lesions in fat-fed Chop&#x2b;/&#x2b;; Apoe&#x2212;/&#x2212; and Chop&#x2212;/&#x2212;; Apoe&#x2212;/&#x2212; mice, they found that plaques and apoptotic cells were reduced in CHOP-deficient mice. They suggest that the CHOP pathway may serve as a potential therapeutic target for treating atherosclerosis (<xref ref-type="bibr" rid="B70">Thorp et al., 2009</xref>).</p>
<p>Ebru Erbay and colleagues discovered through genetic and chemical models that adipocyte fatty acid-binding protein 4 (aP2) is a major regulatory factor for lipid-induced endoplasmic reticulum stress in macrophages. They found that upregulating the chemical chaperone 4-phenyl butyric acid (PBA) or inhibiting the lipid chaperone aP2 significantly suppressed endoplasmic reticulum stress, cell death, and atherosclerosis in macrophages (<xref ref-type="bibr" rid="B18">Erbay et al., 2009</xref>).</p>
<p>Masafumi Myoishi, MD and colleagues detected the expression of endoplasmic reticulum (ER) chaperones and apoptotic cells in smooth muscle cells and macrophages within thin-cap fibroatheromas and ruptured plaques in coronary artery segments obtained during autopsies of 71 patients. They found a significant increase in ER chaperone expression and apoptotic cells. Oxysterols, such as 7-ketocholesterol (7-KC), contribute to the cytotoxicity of oxidized low-density lipoprotein. The upregulation of 7-KC expression induces ER chaperone upregulation through the generation of reactive oxygen species, leading to increased endoplasmic reticulum stress and activation of the downstream CHOP signaling pathway, which induces apoptosis in smooth muscle cells and macrophages. Further experiments revealed the activation of the Chop-dependent pathway in unstable plaques. Therefore, endoplasmic reticulum stress is considered one of the factors that increase vulnerability of coronary artery plaques, leading to acute coronary syndrome and fatal outcomes in patients with coronary artery disease (<xref ref-type="bibr" rid="B51">Myoishi et al., 2007</xref>).</p>
<p>G&#xf6;khans S. Hotamisligil reviewed the cross-talk between the endoplasmic reticulum (ER) stress response and inflammatory pathways in the context of metabolic homeostasis and disease, highlighting the importance of ER stress as a crucial mechanism underlying metabolic diseases. The author proposed that ER stress-induced inflammation and autophagy are also significant causes of metabolic dysfunction. By summarizing these viewpoints, the author suggested that there is enormous potential for targeting ER stress in the treatment of metabolic diseases (<xref ref-type="bibr" rid="B28">Hotamisligil, 2010a</xref>).</p>
<p>Ira Tabas provided a comprehensive review on the molecular mechanisms of endoplasmic reticulum (ER) stress and cell apoptosis, focusing on the pathophysiological relationship between ER stress and cell apoptosis, as well as the integration and complementarity of various cell apoptosis pathways induced by ER stress. The aim was to provide a basis for future drug intervention strategies (<xref ref-type="bibr" rid="B67">Tabas and Ron, 2011</xref>). David Ron and colleagues systematically discussed the three branches of the unfolded protein response (UPR) under ER stress and explained the role of different gene expressions in the secretion pathway. The goal was to preserve the beneficial effects of ER stress in the human body while alleviating its detrimental effects (<xref ref-type="bibr" rid="B57">Ron and Walter, 2007</xref>).</p>
<p>G&#xf6;khan S. Hotamisligil highlighted the role of endoplasmic reticulum (ER) stress in macrophages exposed to lipotoxic environments, which can activate inflammatory and apoptotic pathways, promoting the formation of atheromatous plaques or accelerating the rupture of vascular plaques and exacerbating metabolic dysfunction. The author proposed that inhibiting or genetically deleting lipid chaperone aP2 could be an important means of enhancing ER folding capacity to alleviate ER stress (<xref ref-type="bibr" rid="B29">Hotamisligil, 2010b</xref>). Mete Civelek and colleagues found through experiments that chronic ER stress and UPR response in endothelial cells were generally present in susceptible sites of atherosclerosis <italic>in vivo</italic>. Further research showed that downstream signaling pathways IRE1 and ATF6, as well as their downstream effectors, were activated by the UPR pathway induced by ER stress. Increasing protein folding capacity to alleviate ER stress may be a feasible method for treating atherosclerosis (<xref ref-type="bibr" rid="B12">Civelek et al., 2009</xref>). Tracie DeVries-Seimon and colleagues found through experiments that free cholesterol loading in macrophages could induce ER stress, activate p38-CHOP and JNK2 pathways, and induce cell apoptosis, which required the involvement of type A scavenger receptor (SRA) (<xref ref-type="bibr" rid="B14">Devries-Seimon et al., 2005</xref>).</p>
<p>The top ten highly cited publications reflect the high academic standards in the field of research on ERS and AS, serving as a crucial knowledge repository. These publications summarize both basic and clinical research findings, providing evidence and guidance for future investigations. Seven of them focused on the pathological mechanisms by which ERS promotes the progression of AS, while three focused on the potential of targeting ERS in treating AS, indicating that the pathological mechanisms of ERS and AS are the primary research issues.</p>
</sec>
<sec id="s4-3">
<title>4.3 Identification of research hotspots and emerging topics</title>
<p>In bibliometrics, keyword co-occurrence analysis reflects the research hotspots and development trends in the field. A timeline visualization shows the trend of research hotspots over time, while keyword burst analysis helps to track research frontiers. Keyword clustering analysis displays research modules and knowledge structures.</p>
<p>From the keyword co-occurrence map (<xref ref-type="fig" rid="F9">Figure 9A</xref>) and <xref ref-type="table" rid="T6">Table 6</xref>, it can be observed that keywords such as apoptosis, oxidative stress, unfolded protein response, inflammation, vascular endothelial cell, smooth muscle cells, NF-&#x3ba;B, macrophage, etc. represent the main research directions and have constructed the knowledge structure of this field. The appearance of vascular endothelial cells, risk factors, plasma homocysteine, cystathionine beta synthase, and pancreatic beta cells from 2000 to 2005 indicated the initial focus of research. The subsequent appearance of keywords such as e deficient mice, metabolic syndrome, mice, mechanisms, differentiation, signaling pathway, cholesterol efflux, etc. enriched the knowledge base of ERS and AS fields. With the continuous improvement and innovation of experimental techniques, numerous scholars have conducted more in-depth and diversified research on the cellular and molecular mechanisms in the ERS and AS fields. In recent 5&#xa0;years, related studies such as vascular calcification, endothelial dysfunction, NLRP3 inflammation, ischemia-reperfusion injury, and heart failure have become new hotspots, and are currently in a burst phase.</p>
<p>Through keyword clustering analysis, we can gain a more intuitive understanding of the main directions in the field of ERS and AS over the past 20 years. The figure displays a total of 10 clusters, and based on the content of keywords within each cluster, we categorized them into three main research directions.</p>
<sec id="s4-3-1">
<title>4.3.1 The pro-atherosclerotic effects of ER stress on different cells</title>
<p>Endothelial cells, macrophages, and smooth muscle cells are all related to the occurrence and development of atherosclerosis. The dysfunction of endothelial cells, polarization of macrophages, and apoptosis and migration of smooth muscle cells all contribute to the occurrence and progression of atherosclerosis. Vascular endothelial cells (VECs) are the barrier between the vascular wall and blood circulation and are important cells for maintaining the stability of the vascular wall (<xref ref-type="bibr" rid="B33">Kr&#xfc;ger-Genge et al., 2019</xref>). Endothelial dysfunction is the initiating factor of atherosclerosis. Atherosclerosis often occurs in areas with turbulent blood flow, where endothelial cells are subjected to continuous blood flow strain. Unstable blood flow shear stress is a significant contributor to endothelial dysfunction, capable of directly inducing AS. (<xref ref-type="bibr" rid="B11">Chung et al., 2015</xref>). Oxidized low-density lipoprotein and homocysteine are independent risk factors for atherosclerosis and can directly induce ERS in VECs (<xref ref-type="bibr" rid="B47">Lubrano and Balzan, 2014</xref>; <xref ref-type="bibr" rid="B30">Ji et al., 2021</xref>). Excessive ERS will activate pro-apoptotic pathways and recruit inflammatory factors. HANG et al. found that in ox-LDL-induced human aortic endothelial cells (HAECs), ERS-related proteins such as CHOP, p-PERK, GRP78, NLRP3, and interleukin-1&#x3b2; were upregulated, suggesting that ERS induces VECs apoptosis and mediates inflammation to promote endothelial dysfunction (<xref ref-type="bibr" rid="B24">Hang et al., 2020</xref>). Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS). It competes with L-arginine for binding to the active site of NOS, reducing the production of nitric oxide (NO) and promoting the generation of reactive oxygen species (ROS). ADMA has been shown to be closely associated with atherosclerosis (AS) (<xref ref-type="bibr" rid="B37">Lee et al., 2021</xref>). Interestingly, in the experiment conducted by Toyomasu et al., it was found that levels of homocysteine (Hcy) and ADMA were highly correlated (<xref ref-type="bibr" rid="B72">Toyomasu et al., 2021</xref>). Elevated levels of Hcy can increase ADMA levels through the induction of oxidative stress (<xref ref-type="bibr" rid="B19">Esse et al., 2019</xref>), which in turn stimulates endothelial cell endoplasmic reticulum stress (ERS) and leads to endothelial dysfunction. Activated and dysfunctional endothelial cells promote the upregulation of adhesion molecules and chemokines, as well as the secretion of vascular endothelial growth factor, resulting in the formation of lipid plaques and vascular remodeling. Additionally, the inflammatory state of endothelial cells exacerbates plaque instability (<xref ref-type="bibr" rid="B49">Milutinovi&#x107; et al., 2020</xref>; <xref ref-type="bibr" rid="B6">Bj&#xf6;rkegren and Lusis, 2022</xref>). Increasing evidence suggests that sustained ERS caused by various factors leading to changes in the intracellular and extracellular environment of endothelial cells is an important mechanism underlying endothelial dysfunction. The role of ERS-induced unfolded protein response (UPR) in promoting apoptosis and activating inflammatory responses in endothelial dysfunction has drawn the attention of many researchers.</p>
<p>Macrophages are the main effector cells in the occurrence and progression of AS (<xref ref-type="bibr" rid="B50">Moore and Tabas, 2011</xref>). Studies have also shown that ERS-induced macrophage apoptosis is a key factor in plaque vulnerability and rupture (<xref ref-type="bibr" rid="B51">Myoishi et al., 2007</xref>). Numerous experimental studies have demonstrated that ERS-related protein expression is upregulated in macrophages from rat models at all stages of AS (<xref ref-type="bibr" rid="B14">Devries-Seimon et al., 2005</xref>; <xref ref-type="bibr" rid="B82">Zhou et al., 2005</xref>), with UPR-mediated activation of CHOP and downstream apoptotic signaling pathways being one of the most common mechanisms underlying ERS-induced macrophage apoptosis (<xref ref-type="bibr" rid="B4">Battson et al., 2017</xref>). Wu et al. (<xref ref-type="bibr" rid="B75">Wu et al., 2018</xref>) found that ox-LDL induces macrophage secretion of high mobility group B-1 (HMGB-1) through oxidative stress, and HMGB-1 promotes macrophage apoptosis and foam cell formation by activating the CHOP pathway. In addition, ox-LDL can induce upregulation of scavenger receptors CD36 and SR-A through ERS induction (<xref ref-type="bibr" rid="B78">Yao S. et al., 2014</xref>; <xref ref-type="bibr" rid="B10">Choroma&#x144;ska et al., 2017</xref>; <xref ref-type="bibr" rid="B31">Kattoor et al., 2019</xref>). Meanwhile, activation of UPR signaling pathways downregulates expression of ABCA1, ABCG1, and SR-BI, reducing cholesterol efflux, affecting macrophage lipid metabolism, and promoting macrophage phenotypic transformation into foam cells. Foam cell formation is the most important pathological hallmark of the entire AS process (<xref ref-type="bibr" rid="B80">Yao ST. et al., 2014</xref>). Yao et al. (<xref ref-type="bibr" rid="B80">Yao ST. et al., 2014</xref>) found that minimally modified low-density lipoprotein (mm-LDL) induces the accumulation of free cholesterol (FC) in the endoplasmic reticulum (ER), stimulating macrophage ERS and activating the ATF6 and p-IRE1-mediated UPR signaling pathway through Toll-like receptor 4 (TLR4). This leads to activation of JNK and p38-CHOP-Bax-mediated apoptosis, promoting cell death and plaque instability. In addition, research results have also indicated a close association between ERS and the regulation of macrophage polarization in inflammatory diseases such as atherosclerosis, tumors, and pulmonary fibrosis (<xref ref-type="bibr" rid="B54">Oh et al., 2012</xref>; <xref ref-type="bibr" rid="B13">Cook et al., 2016</xref>). Studies have shown that all three pathways of UPR activated by ERS can be associated with M1 polarization of macrophages through downstream factors such as JNK-AP1 and NF-&#x3ba;B, regulating macrophage polarization towards M1 and inducing inflammatory responses (<xref ref-type="bibr" rid="B32">Ke et al., 2017</xref>). Through the study of macrophage subtypes in plaques, CHO found that M2-type macrophages are highly distributed in stable plaques, while M1-type macrophages are predominant in unstable plaques, especially in the shoulder region of the intima prone to rupture (<xref ref-type="bibr" rid="B9">Cho et al., 2013</xref>). The above research results suggest that ERS induces macrophage polarization towards M1, resulting in high expression of M1-type macrophages and promoting plaque rupture.</p>
<p>ERS-induced apoptosis of vascular smooth muscle cells (VSMCs) leads to thinning of the protective fibrous cap and may be one of the important mechanisms contributing to the transition of atherosclerotic plaques from stable to unstable (<xref ref-type="bibr" rid="B79">Yao et al., 2012</xref>; <xref ref-type="bibr" rid="B45">Liu et al., 2016</xref>). Protein kinase C (PKC) is a key regulatory factor in VSMC apoptosis and can participate in ERS-dependent apoptotic signaling through the IRE1&#x3b1;/JNK pathway (<xref ref-type="bibr" rid="B34">Larroque-Cardoso et al., 2013</xref>). Vascular calcification is a prominent feature of atherosclerosis, and experimental evidence suggests that elevated expression of GRP78 in calcified arteries indicates that ERS promotes the phenotypic transformation of VSMCs into osteoblast-like cells, leading to vascular calcification (<xref ref-type="bibr" rid="B15">Duan et al., 2009</xref>). In addition, hyperhomocysteinemia (HHcy) can also significantly activate the arm of endoplasmic reticulum protein (HERP) in VSMCs, inducing VSMC phenotype transformation (<xref ref-type="bibr" rid="B42">Lin et al., 2018</xref>).</p>
<p>The mechanisms by which ERS promotes atherosclerosis in different cell types are complex and involve various physiological and pathological responses, including apoptosis, inflammatory reactions, oxidative stress, and disturbances in lipid metabolism. Therefore, ERS is also a hot and focal point of research.</p>
</sec>
<sec id="s4-3-2">
<title>4.3.2 Mechanisms underlying the promotion of AS by ERS</title>
<p>It is known that the unfolded protein response (UPR) is an adaptive response to perturbations in endoplasmic reticulum (ER) homeostasis caused by various pathological factors. The primary goal of the UPR is to adjust and restore ER function through inhibition of translation, upregulation of ER chaperones, and degradation of unfolded proteins (<xref ref-type="bibr" rid="B17">Engin and Hotamisligil, 2010</xref>). Persistent ERS can lead to the activation of apoptotic and inflammatory pathways. C/EBP homologous protein (CHOP), a widely studied biomarker of ERS-related apoptotic signaling pathways, induces apoptosis by upregulating the expression of members of the Bcl-2 family to activate the apoptotic signaling pathway mediated by CHOP. In addition, the activated IRE1 binds to TNF receptor-associated factor 2 (TRAF2) to form a complex that activates JNK and p38 MAPK via the apoptotic signal-regulating kinase 1 (ASK1), which also induces apoptosis (<xref ref-type="bibr" rid="B27">Hong et al., 2017</xref>). At the same time, ERS activates inflammatory pathways through various signaling pathways, activating the NLRP3 inflammasome and recruiting large amounts of inflammatory factors such as IL-8, IL-6, monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-&#x3b1; (TNF-&#x3b1;), triggering inflammatory responses (<xref ref-type="bibr" rid="B38">Li et al., 2005</xref>). ERS-mediated apoptosis and inflammatory responses are widely involved in all stages of atherosclerosis.</p>
<p>Insulin resistance (IR) is recognized as a key pathogenic factor and a major cause of various metabolic abnormalities associated with cardiovascular diseases (<xref ref-type="bibr" rid="B76">Yan, 2005</xref>). IR can mediate changes in C-peptide and adiponectin levels, leading to dysregulation of lipid metabolism and promoting the development of atherosclerosis (<xref ref-type="bibr" rid="B44">Linna and Lifeng, 2017</xref>). Due to impaired pancreatic function accompanying IR, the body enters a state of hyperglycemia. This activates signaling pathways such as polyols, hexosamines, advanced glycation end products, and protein kinase C, enhancing the activity of reduced nicotinamide adenine dinucleotide phosphate oxidase, resulting in the generation of a large number of reactive oxygen species (ROS). This leads to increased oxidative stress levels, affects endoplasmic reticulum (ER) homeostasis, activates ER stress (ERS) (<xref ref-type="bibr" rid="B43">Lindholm et al., 2017</xref>), and mediates high expression of inflammatory factors such as NF-&#x3ba;B, TNF-&#x3b1;, matrix metalloproteinases, causing endothelial dysfunction, collagen fiber proliferation, and smooth muscle cell apoptosis. Interestingly, under the influence of IR, macrophages become more sensitive to ER stress, activating inflammatory responses and apoptotic signaling pathways, thereby promoting the progression of atherosclerosis (<xref ref-type="bibr" rid="B60">Schmitz et al., 2018</xref>).</p>
<p>Numerous experimental studies have found that endoplasmic reticulum stress (ERS) can promote macrophage apoptosis in advanced stage atherosclerotic (AS) lesions, and it has been discovered that ERS-induced macrophage apoptosis requires the involvement of scavenger receptor A (SRA) (<xref ref-type="bibr" rid="B20">Feng et al., 2003a</xref>; <xref ref-type="bibr" rid="B65">Tabas, 2005</xref>; <xref ref-type="bibr" rid="B41">Lim et al., 2008</xref>). Scavenger receptors are mainly expressed on the surface of macrophages in different tissues and organs and mediate lipid internalization by recognizing changes in the surface molecular patterns of chemically modified low-density lipoprotein, thereby forming foam cells (<xref ref-type="bibr" rid="B63">Suzuki et al., 1997</xref>). Macrophages at the early stage of arterial atherosclerotic lesion damage have normal cholesterol transport capabilities. Cholesterol taken up by the surface scavenger receptor can be esterified into fatty acids in the endoplasmic reticulum through acyl-CoA: cholesterol acyltransferase (ACAT) and transferred out of the cell membrane or to the extracellular space (<xref ref-type="bibr" rid="B64">Tabas, 2000</xref>). However, in late-stage injury, both ACAT activity and cholesterol efflux function of macrophages are impaired, leading to the accumulation of a large amount of free cholesterol (FC) (<xref ref-type="bibr" rid="B61">Shio et al., 1979</xref>; <xref ref-type="bibr" rid="B62">Small et al., 1984</xref>). The accumulation of FC can activate the unfolded protein response (UPR) and its downstream apoptotic signaling pathways, causing macrophage apoptosis (<xref ref-type="bibr" rid="B20">Feng et al., 2003a</xref>; <xref ref-type="bibr" rid="B21">Feng et al., 2003b</xref>).</p>
</sec>
<sec id="s4-3-3">
<title>4.3.3 Diseases associated with ERS and AS</title>
<p>AS is a significant pathological basis for vascular diseases worldwide. The progression of AS leads to gradual narrowing of the lumen, resulting in blood flow obstruction, as well as unstable plaque rupture leading to acute thrombosis and subsequent ischemic necrosis of affected organs, which is a major cause of sudden death. Its main clinical manifestations include ischemic heart disease (IHD), ischemic stroke, and peripheral arterial disease (<xref ref-type="bibr" rid="B25">Herrington et al., 2016</xref>). Additionally, the incidence of AS increases with age. Furthermore, ERS plays a role in diseases such as non-alcoholic fatty liver disease (NAFLD) and Alzheimer&#x2019;s disease and is closely associated with the development of AS. As a metabolic disease, NAFLD is closely related to oxidative stress and ERS (<xref ref-type="bibr" rid="B3">Ashraf and Sheikh, 2015</xref>). ERS activates the PERK-eIF2&#x3b1; pathway, regulates lipid synthesis and degeneration, increases <italic>de novo</italic> lipogenesis, and promotes lipid deposition in liver cells (<xref ref-type="bibr" rid="B71">Tian et al., 2018</xref>). The severity of hepatic steatosis can predict the risk of future cardiovascular events (<xref ref-type="bibr" rid="B55">Pisto et al., 2014</xref>). Multiple studies have reported that NAFLD patients have a significantly higher risk of developing coronary heart disease, and the most common cause of death in NAFLD patients is cardiovascular disease (CVD) (<xref ref-type="bibr" rid="B69">Targher et al., 2016</xref>; <xref ref-type="bibr" rid="B22">Golabi et al., 2019</xref>). The pathological mechanism of AD involves abnormal extracellular deposition of &#x3b2;-amyloid protein in the brain, leading to the destruction of surrounding neurons and synapses (<xref ref-type="bibr" rid="B52">Nebel et al., 2018</xref>). It has been discovered that the abnormal accumulation of A&#x3b2; induces ERS and activates the UPR and its downstream signaling pathways, upregulating NF-&#x3ba;B to activate glial cells, induce neuroinflammation, and exacerbate the progression of AD (<xref ref-type="bibr" rid="B59">Salminen et al., 2020</xref>). On the other hand, AS can promote the accumulation of &#x3b2;-amyloid protein in the brain by reducing cerebral blood flow and causing cerebral hypoxia (<xref ref-type="bibr" rid="B48">Matthews et al., 2019</xref>; <xref ref-type="bibr" rid="B68">Takousis et al., 2019</xref>). In turn, A&#x3b2; promotes the progression of AS through endothelial dysfunction, oxidative stress, and inflammatory responses (<xref ref-type="bibr" rid="B23">Gupta and Iadecola, 2015</xref>; <xref ref-type="bibr" rid="B46">Liu et al., 2019</xref>), forming a vicious cycle. Research on diseases related to ERS and AS is also a hot topic of study.</p>
<p>Our findings reveal that the mechanistic study of ERS and AS has been a hot topic of research, and the enthusiasm of scholars in the study of related diseases has continued to rise with the passage of time. Although significant progress has been made in ERS and AS related research, it is found through our study that further research is still needed in this field to fill some knowledge gaps: a. The mechanisms related to ERS-induced inflammatory response and activation of apoptotic pathway to promote the progression of AS are relatively well established, while there are relatively few data related to biological targets that modulate or restore the function of ER. b. As shown by the results of the present study, the vast majority of the highly co-cited literature are basic research or review articles, while influential clinical trials and practice guidelines are quite lacking, suggesting that the research results in this field have not fully realized the widespread application from laboratory to clinic. Meanwhile, through the trend of research hotspots over time and the gaps found in this study, we can speculate the future research trends in this field: a. Research on the microscopic mechanism of ERS and AS. b. Screening of biological targets to modulate the function of ER or inhibit ERS and determination of their clinical effects. c. The treatment of diseases related to ERS and AS, as well as the development of new drugs targeting corresponding targets.</p>
</sec>
</sec>
</sec>
<sec sec-type="conclusion" id="s5">
<title>5 Conclusion</title>
<p>This study utilized CiteSpace, VOSviewer, and the R package of &#x201c;bibliometric&#x201d; to perform a visualized analysis of the literature in the field of ERS and AS, providing an intuitive display of the current research status and frontier hotspots in this field. By collecting relevant literature published between 2000 and 2023, we established a knowledge base of ERS and AS and found that ERS has significant research value in understanding the mechanisms and treatments of AS. Analysis of the collaboration network map revealed that China and the United States are the main countries conducting research on ERS and AS, and Ira Tabas is an eminent figure in this field, with highly influential and academically valuable publications. The authors have formed relatively stable collaborative relationships, but breaking through geographical limitations and strengthening further cooperation is still necessary. Scholars are more focused on studying the pathological mechanisms of ERS in promoting the occurrence and development of AS, as well as related diseases and biomarkers, which will be the key areas of future research attention. While paying attention to basic research, researchers should also emphasize the integration with clinical aspects to provide scientific evidence for the treatment of clinically relevant AS-related diseases.</p>
</sec>
</body>
<back>
<sec id="s6">
<title>Author contributions</title>
<p>XH: Writing&#x2013;original draft, Writing&#x2013;review and editing, Investigation, Methodology, Software, Conceptualization, Data curation, Formal Analysis, Project administration, Resources. FJ: Data curation, Formal Analysis, Validation, Writing&#x2013;original draft. YM: Data curation, Investigation, Methodology, Software, Writing&#x2013;original draft. KZ: Data curation, Formal Analysis, Software, Writing&#x2013;review and editing. ZW: Investigation, Methodology, Project administration, Resources, Writing&#x2013;original draft. ZH: Methodology, Project administration, Software, Writing&#x2013;original draft. JY: Validation, Visualization, Writing&#x2013;original draft, Writing&#x2013;review and editing. LZ: Funding acquisition, Validation, Visualization, Writing&#x2013;review and editing.</p>
</sec>
<sec sec-type="funding-information" id="s7">
<title>Funding</title>
<p>The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. National Natural Science Foundation of China (no: 81974561), 2021 Shandong Province Chinese Medicine Science and Technology Youth Program (no: 2021Q114), Shandong Provincial Natural Science Foundation Doctoral Fund (no: ZR2017BH091, no: ZR2021MH410), China Postdoctoral Science Foundation (no: 2017M612342), 2023 Academic School of &#x2018;Renal Qi Imbalance&#x2019; Traditional Chinese Medicine Characteristic Technology Project, 2019 Shandong Province Health and Health Outstanding Young Talent Project, 2023 Provincial Traditional Chinese Medicine High-level Talent Cultivation Project, Special Funds for Cardiovascular TCM-TaiShan Scholars Engineering.</p>
</sec>
<sec sec-type="COI-statement" id="s8">
<title>Conflict of interest</title>
<p>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</p>
</sec>
<sec sec-type="disclaimer" id="s9">
<title>Publisher&#x2019;s note</title>
<p>All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.</p>
</sec>
<ref-list>
<title>References</title>
<ref id="B1">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Adolph</surname>
<given-names>T. E.</given-names>
</name>
<name>
<surname>Niederreiter</surname>
<given-names>L.</given-names>
</name>
<name>
<surname>Blumberg</surname>
<given-names>R. S.</given-names>
</name>
<name>
<surname>Kaser</surname>
<given-names>A.</given-names>
</name>
</person-group> (<year>2012</year>). <article-title>Endoplasmic reticulum stress and inflammation</article-title>. <source>Dig. Dis.</source> <volume>30</volume> (<issue>4</issue>), <fpage>341</fpage>&#x2013;<lpage>346</lpage>. <pub-id pub-id-type="doi">10.1159/000338121</pub-id>
</citation>
</ref>
<ref id="B2">
<citation citation-type="book">
<person-group person-group-type="author">
<name>
<surname>Aria</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Cuccurullo</surname>
<given-names>C.</given-names>
</name>
<name>
<surname>Egghe</surname>
<given-names>L.</given-names>
</name>
</person-group> (<year>2017</year>). <source>bibliometrix: an R-tool for comprehensive science mapping analysis</source>.</citation>
</ref>
<ref id="B3">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Ashraf</surname>
<given-names>N. U.</given-names>
</name>
<name>
<surname>Sheikh</surname>
<given-names>T. A.</given-names>
</name>
</person-group> (<year>2015</year>). <article-title>Endoplasmic reticulum stress and Oxidative stress in the pathogenesis of Non-alcoholic fatty liver disease</article-title>. <source>Free Radic. Res.</source> <volume>49</volume> (<issue>12</issue>), <fpage>1405</fpage>&#x2013;<lpage>1418</lpage>. <pub-id pub-id-type="doi">10.3109/10715762.2015.1078461</pub-id>
</citation>
</ref>
<ref id="B4">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Battson</surname>
<given-names>M. L.</given-names>
</name>
<name>
<surname>Lee</surname>
<given-names>D. M.</given-names>
</name>
<name>
<surname>Gentile</surname>
<given-names>C. L.</given-names>
</name>
</person-group> (<year>2017</year>). <article-title>Endoplasmic reticulum stress and the development of endothelial dysfunction</article-title>. <source>Am. J. Physiol. Heart Circ. Physiol.</source> <volume>312</volume> (<issue>3</issue>), <fpage>H355</fpage>&#x2013;<lpage>H367</lpage>. <pub-id pub-id-type="doi">10.1152/ajpheart.00437.2016</pub-id>
</citation>
</ref>
<ref id="B5">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Benjamin</surname>
<given-names>E. J.</given-names>
</name>
<name>
<surname>Blaha</surname>
<given-names>M. J.</given-names>
</name>
<name>
<surname>Chiuve</surname>
<given-names>S. E.</given-names>
</name>
<name>
<surname>Cushman</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Das</surname>
<given-names>S. R.</given-names>
</name>
<name>
<surname>Deo</surname>
<given-names>R.</given-names>
</name>
<etal/>
</person-group> (<year>2017</year>). <article-title>Heart disease and stroke statistics-2017 update: a report from the American heart association</article-title>. <source>Circulation</source> <volume>135</volume> (<issue>10</issue>), <fpage>e146</fpage>&#x2013;<lpage>e603</lpage>. <pub-id pub-id-type="doi">10.1161/cir.0000000000000485</pub-id>
</citation>
</ref>
<ref id="B6">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Bj&#xf6;rkegren</surname>
<given-names>J. L. M.</given-names>
</name>
<name>
<surname>Lusis</surname>
<given-names>A. J.</given-names>
</name>
</person-group> (<year>2022</year>). <article-title>Atherosclerosis: recent developments</article-title>. <source>Cell</source> <volume>185</volume> (<issue>10</issue>), <fpage>1630</fpage>&#x2013;<lpage>1645</lpage>. <pub-id pub-id-type="doi">10.1016/j.cell.2022.04.004</pub-id>
</citation>
</ref>
<ref id="B7">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Bravo</surname>
<given-names>R.</given-names>
</name>
<name>
<surname>Vicencio</surname>
<given-names>J. M.</given-names>
</name>
<name>
<surname>Parra</surname>
<given-names>V.</given-names>
</name>
<name>
<surname>Troncoso</surname>
<given-names>R.</given-names>
</name>
<name>
<surname>Munoz</surname>
<given-names>J. P.</given-names>
</name>
<name>
<surname>Bui</surname>
<given-names>M.</given-names>
</name>
<etal/>
</person-group> (<year>2011</year>). <article-title>Increased ER-mitochondrial coupling promotes mitochondrial respiration and bioenergetics during early phases of ER stress</article-title>. <source>J. Cell Sci.</source> <volume>124</volume> (<issue>Pt 13</issue>), <fpage>2143</fpage>&#x2013;<lpage>2152</lpage>. <pub-id pub-id-type="doi">10.1242/jcs.080762</pub-id>
</citation>
</ref>
<ref id="B8">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Chen</surname>
<given-names>C.</given-names>
</name>
</person-group> (<year>2006</year>). <article-title>CiteSpace II: detecting and visualizing emerging trends and transient patterns in scientific literature</article-title>. <source>J. Am. Soc. Inf. Sci. Technol.</source> <volume>57</volume> (<issue>3</issue>), <fpage>359</fpage>&#x2013;<lpage>377</lpage>. <pub-id pub-id-type="doi">10.1002/asi.20317</pub-id>
</citation>
</ref>
<ref id="B9">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Cho</surname>
<given-names>K. Y.</given-names>
</name>
<name>
<surname>Miyoshi</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Kuroda</surname>
<given-names>S.</given-names>
</name>
<name>
<surname>Yasuda</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Kamiyama</surname>
<given-names>K.</given-names>
</name>
<name>
<surname>Nakagawara</surname>
<given-names>J.</given-names>
</name>
<etal/>
</person-group> (<year>2013</year>). <article-title>The phenotype of infiltrating macrophages influences arteriosclerotic plaque vulnerability in the carotid artery</article-title>. <source>J. Stroke Cerebrovasc. Dis.</source> <volume>22</volume> (<issue>7</issue>), <fpage>910</fpage>&#x2013;<lpage>918</lpage>. <pub-id pub-id-type="doi">10.1016/j.jstrokecerebrovasdis.2012.11.020</pub-id>
</citation>
</ref>
<ref id="B10">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Choroma&#x144;ska</surname>
<given-names>B.</given-names>
</name>
<name>
<surname>My&#x15b;liwiec</surname>
<given-names>P.</given-names>
</name>
<name>
<surname>Choroma&#x144;ska</surname>
<given-names>K.</given-names>
</name>
<name>
<surname>Dadan</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Chabowski</surname>
<given-names>A.</given-names>
</name>
</person-group> (<year>2017</year>). <article-title>The role of CD36 receptor in the pathogenesis of atherosclerosis</article-title>. <source>Adv. Clin. Exp. Med.</source> <volume>26</volume> (<issue>4</issue>), <fpage>717</fpage>&#x2013;<lpage>722</lpage>. <pub-id pub-id-type="doi">10.17219/acem/62325</pub-id>
</citation>
</ref>
<ref id="B11">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Chung</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Kim</surname>
<given-names>K. H.</given-names>
</name>
<name>
<surname>Lee</surname>
<given-names>S. C.</given-names>
</name>
<name>
<surname>An</surname>
<given-names>S. H.</given-names>
</name>
<name>
<surname>Kwon</surname>
<given-names>K.</given-names>
</name>
</person-group> (<year>2015</year>). <article-title>Ursodeoxycholic acid (UDCA) exerts anti-atherogenic effects by inhibiting endoplasmic reticulum (ER) stress induced by disturbed flow</article-title>. <source>Mol. Cells</source> <volume>38</volume> (<issue>10</issue>), <fpage>851</fpage>&#x2013;<lpage>858</lpage>. <pub-id pub-id-type="doi">10.14348/molcells.2015.0094</pub-id>
</citation>
</ref>
<ref id="B12">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Civelek</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Manduchi</surname>
<given-names>E.</given-names>
</name>
<name>
<surname>Riley</surname>
<given-names>R. J.</given-names>
</name>
<name>
<surname>Stoeckert</surname>
<given-names>C. J.</given-names>
</name>
<name>
<surname>Davies</surname>
<given-names>P. F.</given-names>
</name>
</person-group> (<year>2009</year>). <article-title>Chronic endoplasmic reticulum stress activates unfolded protein response in arterial endothelium in regions of susceptibility to atherosclerosis</article-title>. <source>Circ. Res.</source> <volume>105</volume> (<issue>5</issue>), <fpage>453</fpage>&#x2013;<lpage>461</lpage>. <pub-id pub-id-type="doi">10.1161/CIRCRESAHA.109.203711</pub-id>
</citation>
</ref>
<ref id="B13">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Cook</surname>
<given-names>K. L.</given-names>
</name>
<name>
<surname>Soto-Pantoja</surname>
<given-names>D. R.</given-names>
</name>
<name>
<surname>Clarke</surname>
<given-names>P. A.</given-names>
</name>
<name>
<surname>Cruz</surname>
<given-names>M. I.</given-names>
</name>
<name>
<surname>Zwart</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>W&#xe4;rri</surname>
<given-names>A.</given-names>
</name>
<etal/>
</person-group> (<year>2016</year>). <article-title>Endoplasmic reticulum stress protein GRP78 modulates lipid metabolism to control drug sensitivity and antitumor immunity in breast cancer</article-title>. <source>Cancer Res.</source> <volume>76</volume> (<issue>19</issue>), <fpage>5657</fpage>&#x2013;<lpage>5670</lpage>. <pub-id pub-id-type="doi">10.1158/0008-5472.CAN-15-2616</pub-id>
</citation>
</ref>
<ref id="B14">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Devries-Seimon</surname>
<given-names>T.</given-names>
</name>
<name>
<surname>Li</surname>
<given-names>Y.</given-names>
</name>
<name>
<surname>Yao</surname>
<given-names>P. M.</given-names>
</name>
<name>
<surname>Stone</surname>
<given-names>E.</given-names>
</name>
<name>
<surname>Wang</surname>
<given-names>Y.</given-names>
</name>
<name>
<surname>Davis</surname>
<given-names>R. J.</given-names>
</name>
<etal/>
</person-group> (<year>2005</year>). <article-title>Cholesterol-induced macrophage apoptosis requires ER stress pathways and engagement of the type A scavenger receptor</article-title>. <source>J. Cell Biol.</source> <volume>171</volume> (<issue>1</issue>), <fpage>61</fpage>&#x2013;<lpage>73</lpage>. <pub-id pub-id-type="doi">10.1083/jcb.200502078</pub-id>
</citation>
</ref>
<ref id="B15">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Duan</surname>
<given-names>X.</given-names>
</name>
<name>
<surname>Zhou</surname>
<given-names>Y.</given-names>
</name>
<name>
<surname>Teng</surname>
<given-names>X.</given-names>
</name>
<name>
<surname>Tang</surname>
<given-names>C.</given-names>
</name>
<name>
<surname>Qi</surname>
<given-names>Y.</given-names>
</name>
</person-group> (<year>2009</year>). <article-title>Endoplasmic reticulum stress-mediated apoptosis is activated in vascular calcification</article-title>. <source>Biochem. Biophys. Res. Commun.</source> <volume>387</volume> (<issue>4</issue>), <fpage>694</fpage>&#x2013;<lpage>699</lpage>. <pub-id pub-id-type="doi">10.1016/j.bbrc.2009.07.085</pub-id>
</citation>
</ref>
<ref id="B16">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Ellegaard</surname>
<given-names>O.</given-names>
</name>
<name>
<surname>Wallin</surname>
<given-names>J. A.</given-names>
</name>
</person-group> (<year>2015</year>). <article-title>The bibliometric analysis of scholarly production: how great is the impact?</article-title> <source>Scientometrics</source> <volume>105</volume> (<issue>3</issue>), <fpage>1809</fpage>&#x2013;<lpage>1831</lpage>. <pub-id pub-id-type="doi">10.1007/s11192-015-1645-z</pub-id>
</citation>
</ref>
<ref id="B17">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Engin</surname>
<given-names>F.</given-names>
</name>
<name>
<surname>Hotamisligil</surname>
<given-names>G. S.</given-names>
</name>
</person-group> (<year>2010</year>). <article-title>Restoring endoplasmic reticulum function by chemical chaperones: an emerging therapeutic approach for metabolic diseases</article-title>. <source>Diabetes Obes. Metab.</source> <volume>12</volume> (<issue>Suppl. 2</issue>), <fpage>108</fpage>&#x2013;<lpage>115</lpage>. <pub-id pub-id-type="doi">10.1111/j.1463-1326.2010.01282.x</pub-id>
</citation>
</ref>
<ref id="B18">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Erbay</surname>
<given-names>E.</given-names>
</name>
<name>
<surname>Babaev</surname>
<given-names>V. R.</given-names>
</name>
<name>
<surname>Mayers</surname>
<given-names>J. R.</given-names>
</name>
<name>
<surname>Makowski</surname>
<given-names>L.</given-names>
</name>
<name>
<surname>Charles</surname>
<given-names>K. N.</given-names>
</name>
<name>
<surname>Snitow</surname>
<given-names>M. E.</given-names>
</name>
<etal/>
</person-group> (<year>2009</year>). <article-title>Reducing endoplasmic reticulum stress through a macrophage lipid chaperone alleviates atherosclerosis</article-title>. <source>Nat. Med.</source> <volume>15</volume> (<issue>12</issue>), <fpage>1383</fpage>&#x2013;<lpage>1391</lpage>. <pub-id pub-id-type="doi">10.1038/nm.2067</pub-id>
</citation>
</ref>
<ref id="B19">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Esse</surname>
<given-names>R.</given-names>
</name>
<name>
<surname>Barroso</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Tavares de Almeida</surname>
<given-names>I.</given-names>
</name>
<name>
<surname>Castro</surname>
<given-names>R.</given-names>
</name>
</person-group> (<year>2019</year>). <article-title>The contribution of homocysteine metabolism disruption to endothelial dysfunction: state-of-the-art</article-title>. <source>Int. J. Mol. Sci.</source> <volume>20</volume> (<issue>4</issue>), <fpage>867</fpage>. <pub-id pub-id-type="doi">10.3390/ijms20040867</pub-id>
</citation>
</ref>
<ref id="B20">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Feng</surname>
<given-names>B.</given-names>
</name>
<name>
<surname>Yao</surname>
<given-names>P. M.</given-names>
</name>
<name>
<surname>Li</surname>
<given-names>Y.</given-names>
</name>
<name>
<surname>Devlin</surname>
<given-names>C. M.</given-names>
</name>
<name>
<surname>Zhang</surname>
<given-names>D.</given-names>
</name>
<name>
<surname>Harding</surname>
<given-names>H. P.</given-names>
</name>
<etal/>
</person-group> (<year>2003a</year>). <article-title>The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages</article-title>. <source>Nat. Cell Biol.</source> <volume>5</volume> (<issue>9</issue>), <fpage>781</fpage>&#x2013;<lpage>792</lpage>. <pub-id pub-id-type="doi">10.1038/ncb1035</pub-id>
</citation>
</ref>
<ref id="B21">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Feng</surname>
<given-names>B.</given-names>
</name>
<name>
<surname>Zhang</surname>
<given-names>D.</given-names>
</name>
<name>
<surname>Kuriakose</surname>
<given-names>G.</given-names>
</name>
<name>
<surname>Devlin</surname>
<given-names>C. M.</given-names>
</name>
<name>
<surname>Kockx</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Tabas</surname>
<given-names>I.</given-names>
</name>
</person-group> (<year>2003b</year>). <article-title>Niemann-Pick C heterozygosity confers resistance to lesional necrosis and macrophage apoptosis in murine atherosclerosis</article-title>. <source>Proc. Natl. Acad. Sci. U. S. A.</source> <volume>100</volume> (<issue>18</issue>), <fpage>10423</fpage>&#x2013;<lpage>10428</lpage>. <pub-id pub-id-type="doi">10.1073/pnas.1732494100</pub-id>
</citation>
</ref>
<ref id="B22">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Golabi</surname>
<given-names>P.</given-names>
</name>
<name>
<surname>Fukui</surname>
<given-names>N.</given-names>
</name>
<name>
<surname>Paik</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Sayiner</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Mishra</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Younossi</surname>
<given-names>Z. M.</given-names>
</name>
</person-group> (<year>2019</year>). <article-title>Mortality risk detected by atherosclerotic cardiovascular disease score in patients with nonalcoholic fatty liver disease</article-title>. <source>Hepatol. Commun.</source> <volume>3</volume> (<issue>8</issue>), <fpage>1050</fpage>&#x2013;<lpage>1060</lpage>. <pub-id pub-id-type="doi">10.1002/hep4.1387</pub-id>
</citation>
</ref>
<ref id="B23">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Gupta</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Iadecola</surname>
<given-names>C.</given-names>
</name>
</person-group> (<year>2015</year>). <article-title>Impaired A&#x3b2; clearance: a potential link between atherosclerosis and Alzheimer&#x2019;s disease</article-title>. <source>Front. Aging Neurosci.</source> <volume>7</volume>, <fpage>115</fpage>. <pub-id pub-id-type="doi">10.3389/fnagi.2015.00115</pub-id>
</citation>
</ref>
<ref id="B24">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Hang</surname>
<given-names>L.</given-names>
</name>
<name>
<surname>Peng</surname>
<given-names>Y.</given-names>
</name>
<name>
<surname>Xiang</surname>
<given-names>R.</given-names>
</name>
<name>
<surname>Li</surname>
<given-names>X.</given-names>
</name>
<name>
<surname>Li</surname>
<given-names>Z.</given-names>
</name>
</person-group> (<year>2020</year>). <article-title>Ox-LDL causes endothelial cell injury through ASK1/NLRP3-mediated inflammasome activation via endoplasmic reticulum stress</article-title>. <source>Drug Des. Devel Ther.</source> <volume>14</volume>, <fpage>731</fpage>&#x2013;<lpage>744</lpage>. <pub-id pub-id-type="doi">10.2147/DDDT.S231916</pub-id>
</citation>
</ref>
<ref id="B25">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Herrington</surname>
<given-names>W.</given-names>
</name>
<name>
<surname>Lacey</surname>
<given-names>B.</given-names>
</name>
<name>
<surname>Sherliker</surname>
<given-names>P.</given-names>
</name>
<name>
<surname>Armitage</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Lewington</surname>
<given-names>S.</given-names>
</name>
</person-group> (<year>2016</year>). <article-title>Epidemiology of atherosclerosis and the potential to reduce the global burden of atherothrombotic disease</article-title>. <source>Circ. Res.</source> <volume>118</volume> (<issue>4</issue>), <fpage>535</fpage>&#x2013;<lpage>546</lpage>. <pub-id pub-id-type="doi">10.1161/CIRCRESAHA.115.307611</pub-id>
</citation>
</ref>
<ref id="B26">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Hetz</surname>
<given-names>C.</given-names>
</name>
</person-group> (<year>2012</year>). <article-title>The unfolded protein response: controlling cell fate decisions under ER stress and beyond</article-title>. <source>Nat. Rev. Mol. Cell Biol.</source> <volume>13</volume> (<issue>2</issue>), <fpage>89</fpage>&#x2013;<lpage>102</lpage>. <pub-id pub-id-type="doi">10.1038/nrm3270</pub-id>
</citation>
</ref>
<ref id="B27">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Hong</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Kim</surname>
<given-names>K.</given-names>
</name>
<name>
<surname>Kim</surname>
<given-names>J. H.</given-names>
</name>
<name>
<surname>Park</surname>
<given-names>Y.</given-names>
</name>
</person-group> (<year>2017</year>). <article-title>The role of endoplasmic reticulum stress in cardiovascular disease and exercise</article-title>. <source>Int. J. Vasc. Med.</source> <volume>2017</volume>, <fpage>2049217</fpage>. <pub-id pub-id-type="doi">10.1155/2017/2049217</pub-id>
</citation>
</ref>
<ref id="B28">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Hotamisligil</surname>
<given-names>G. S.</given-names>
</name>
</person-group> (<year>2010a</year>). <article-title>Endoplasmic reticulum stress and the inflammatory basis of metabolic disease</article-title>. <source>Cell</source> <volume>140</volume> (<issue>6</issue>), <fpage>900</fpage>&#x2013;<lpage>917</lpage>. <pub-id pub-id-type="doi">10.1016/j.cell.2010.02.034</pub-id>
</citation>
</ref>
<ref id="B29">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Hotamisligil</surname>
<given-names>G. S.</given-names>
</name>
</person-group> (<year>2010b</year>). <article-title>Endoplasmic reticulum stress and atherosclerosis</article-title>. <source>Nat. Med.</source> <volume>16</volume> (<issue>4</issue>), <fpage>396</fpage>&#x2013;<lpage>399</lpage>. <pub-id pub-id-type="doi">10.1038/nm0410-396</pub-id>
</citation>
</ref>
<ref id="B30">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Ji</surname>
<given-names>C.</given-names>
</name>
<name>
<surname>Yi</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Huang</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Zhang</surname>
<given-names>W.</given-names>
</name>
<name>
<surname>Zheng</surname>
<given-names>M.</given-names>
</name>
</person-group> (<year>2021</year>). <article-title>Propofol alleviates inflammation and apoptosis in HCY-induced HUVECs by inhibiting endoplasmic reticulum stress</article-title>. <source>Mol. Med. Rep.</source> <volume>23</volume> (<issue>5</issue>), <fpage>333</fpage>. <pub-id pub-id-type="doi">10.3892/mmr.2021.11972</pub-id>
</citation>
</ref>
<ref id="B31">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Kattoor</surname>
<given-names>A. J.</given-names>
</name>
<name>
<surname>Goel</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Mehta</surname>
<given-names>J. L.</given-names>
</name>
</person-group> (<year>2019</year>). <article-title>LOX-1: regulation, signaling and its role in atherosclerosis</article-title>. <source>Antioxidants (Basel)</source> <volume>8</volume> (<issue>7</issue>), <fpage>218</fpage>. <pub-id pub-id-type="doi">10.3390/antiox8070218</pub-id>
</citation>
</ref>
<ref id="B32">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Ke</surname>
<given-names>D.</given-names>
</name>
<name>
<surname>Yan-zhu</surname>
<given-names>P.</given-names>
</name>
<name>
<surname>Xin</surname>
<given-names>Z.</given-names>
</name>
<name>
<surname>Ming-yan</surname>
<given-names>L.</given-names>
</name>
</person-group> (<year>2017</year>). <article-title>Progress of endoplasmic reticulum stress and macrophage M1/M2polarization</article-title>. <source>Adv. Anatomical Sci. Univ.</source> <volume>23</volume> (<issue>02</issue>), <fpage>201</fpage>&#x2013;<lpage>203&#x2b;7</lpage>. <pub-id pub-id-type="doi">10.16695/j.cnki.1006-2947.2017.02.025</pub-id>
</citation>
</ref>
<ref id="B33">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Kr&#xfc;ger-Genge</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Blocki</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Franke</surname>
<given-names>R. P.</given-names>
</name>
<name>
<surname>Jung</surname>
<given-names>F.</given-names>
</name>
</person-group> (<year>2019</year>). <article-title>Vascular endothelial cell Biology: an update</article-title>. <source>Int. J. Mol. Sci.</source> <volume>20</volume> (<issue>18</issue>), <fpage>4411</fpage>. <pub-id pub-id-type="doi">10.3390/ijms20184411</pub-id>
</citation>
</ref>
<ref id="B34">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Larroque-Cardoso</surname>
<given-names>P.</given-names>
</name>
<name>
<surname>Swiader</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Ingueneau</surname>
<given-names>C.</given-names>
</name>
<name>
<surname>N&#xe8;gre-Salvayre</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Elbaz</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Reyland</surname>
<given-names>M. E.</given-names>
</name>
<etal/>
</person-group> (<year>2013</year>). <article-title>Role of protein kinase C &#x3b4; in ER stress and apoptosis induced by oxidized LDL in human vascular smooth muscle cells</article-title>. <source>Cell Death Dis.</source> <volume>4</volume> (<issue>2</issue>), <fpage>e520</fpage>. <pub-id pub-id-type="doi">10.1038/cddis.2013.47</pub-id>
</citation>
</ref>
<ref id="B35">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Lawrence de Koning</surname>
<given-names>A. B.</given-names>
</name>
<name>
<surname>Werstuck</surname>
<given-names>G. H.</given-names>
</name>
<name>
<surname>Zhou</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Austin</surname>
<given-names>R. C.</given-names>
</name>
</person-group> (<year>2003</year>). <article-title>Hyperhomocysteinemia and its role in the development of atherosclerosis</article-title>. <source>Clin. Biochem.</source> <volume>36</volume> (<issue>6</issue>), <fpage>431</fpage>&#x2013;<lpage>441</lpage>. <pub-id pub-id-type="doi">10.1016/s0009-9120(03)00062-6</pub-id>
</citation>
</ref>
<ref id="B36">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Lebeaupin</surname>
<given-names>C.</given-names>
</name>
<name>
<surname>Vall&#xe9;e</surname>
<given-names>D.</given-names>
</name>
<name>
<surname>Hazari</surname>
<given-names>Y.</given-names>
</name>
<name>
<surname>Hetz</surname>
<given-names>C.</given-names>
</name>
<name>
<surname>Chevet</surname>
<given-names>E.</given-names>
</name>
<name>
<surname>Bailly-Maitre</surname>
<given-names>B.</given-names>
</name>
</person-group> (<year>2018</year>). <article-title>Endoplasmic reticulum stress signalling and the pathogenesis of non-alcoholic fatty liver disease</article-title>. <source>J. Hepatol.</source> <volume>69</volume> (<issue>4</issue>), <fpage>927</fpage>&#x2013;<lpage>947</lpage>. <pub-id pub-id-type="doi">10.1016/j.jhep.2018.06.008</pub-id>
</citation>
</ref>
<ref id="B37">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Lee</surname>
<given-names>T. S.</given-names>
</name>
<name>
<surname>Lu</surname>
<given-names>T. M.</given-names>
</name>
<name>
<surname>Chen</surname>
<given-names>C. H.</given-names>
</name>
<name>
<surname>Guo</surname>
<given-names>B. C.</given-names>
</name>
<name>
<surname>Hsu</surname>
<given-names>C. P.</given-names>
</name>
</person-group> (<year>2021</year>). <article-title>Hyperuricemia induces endothelial dysfunction and accelerates atherosclerosis by disturbing the asymmetric dimethylarginine/dimethylarginine dimethylaminotransferase 2 pathway</article-title>. <source>Redox Biol.</source> <volume>46</volume>, <fpage>102108</fpage>. <pub-id pub-id-type="doi">10.1016/j.redox.2021.102108</pub-id>
</citation>
</ref>
<ref id="B38">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Li</surname>
<given-names>Y.</given-names>
</name>
<name>
<surname>Schwabe</surname>
<given-names>R. F.</given-names>
</name>
<name>
<surname>DeVries-Seimon</surname>
<given-names>T.</given-names>
</name>
<name>
<surname>Yao</surname>
<given-names>P. M.</given-names>
</name>
<name>
<surname>Gerbod-Giannone</surname>
<given-names>M. C.</given-names>
</name>
<name>
<surname>Tall</surname>
<given-names>A. R.</given-names>
</name>
<etal/>
</person-group> (<year>2005</year>). <article-title>Free cholesterol-loaded macrophages are an abundant source of tumor necrosis factor-alpha and interleukin-6: model of NF-kappaB- and map kinase-dependent inflammation in advanced atherosclerosis</article-title>. <source>J. Biol. Chem.</source> <volume>280</volume> (<issue>23</issue>), <fpage>21763</fpage>&#x2013;<lpage>21772</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.M501759200</pub-id>
</citation>
</ref>
<ref id="B39">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Libby</surname>
<given-names>P.</given-names>
</name>
<name>
<surname>Buring</surname>
<given-names>J. E.</given-names>
</name>
<name>
<surname>Badimon</surname>
<given-names>L.</given-names>
</name>
<name>
<surname>Hansson</surname>
<given-names>G. K.</given-names>
</name>
<name>
<surname>Deanfield</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Bittencourt</surname>
<given-names>M. S.</given-names>
</name>
<etal/>
</person-group> (<year>2019</year>). <article-title>Atherosclerosis</article-title>. <source>Nat. Rev. Dis. Prim.</source> <volume>5</volume> (<issue>1</issue>), <fpage>56</fpage>. <pub-id pub-id-type="doi">10.1038/s41572-019-0106-z</pub-id>
</citation>
</ref>
<ref id="B40">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Lijun</surname>
<given-names>Y.</given-names>
</name>
<name>
<surname>Liangxiu</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Naxin</surname>
<given-names>L.</given-names>
</name>
</person-group> (<year>2019</year>). <article-title>A new approach to journal co-citation matrix construction based on the number of co-cited articles in journals</article-title>. <source>Scientometrics</source> <volume>120</volume> (<issue>2</issue>), <fpage>507</fpage>&#x2013;<lpage>517</lpage>. <pub-id pub-id-type="doi">10.1007/s11192-019-03141-9</pub-id>
</citation>
</ref>
<ref id="B41">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Lim</surname>
<given-names>W. S.</given-names>
</name>
<name>
<surname>Timmins</surname>
<given-names>J. M.</given-names>
</name>
<name>
<surname>Seimon</surname>
<given-names>T. A.</given-names>
</name>
<name>
<surname>Sadler</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Kolodgie</surname>
<given-names>F. D.</given-names>
</name>
<name>
<surname>Virmani</surname>
<given-names>R.</given-names>
</name>
<etal/>
</person-group> (<year>2008</year>). <article-title>Signal transducer and activator of transcription-1 is critical for apoptosis in macrophages subjected to endoplasmic reticulum stress <italic>in vitro</italic> and in advanced atherosclerotic lesions <italic>in vivo</italic>
</article-title>. <source>Circulation</source> <volume>117</volume> (<issue>7</issue>), <fpage>940</fpage>&#x2013;<lpage>951</lpage>. <pub-id pub-id-type="doi">10.1161/CIRCULATIONAHA.107.711275</pub-id>
</citation>
</ref>
<ref id="B42">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Lin</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Ni</surname>
<given-names>T.</given-names>
</name>
<name>
<surname>Zhang</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Meng</surname>
<given-names>L.</given-names>
</name>
<name>
<surname>Gao</surname>
<given-names>F.</given-names>
</name>
<name>
<surname>Pan</surname>
<given-names>S.</given-names>
</name>
<etal/>
</person-group> (<year>2018</year>). <article-title>Knockdown of Herp alleviates hyperhomocysteinemia mediated atherosclerosis through the inhibition of vascular smooth muscle cell phenotype switching</article-title>. <source>Int. J. Cardiol.</source> <volume>269</volume>, <fpage>242</fpage>&#x2013;<lpage>249</lpage>. <pub-id pub-id-type="doi">10.1016/j.ijcard.2018.07.043</pub-id>
</citation>
</ref>
<ref id="B43">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Lindholm</surname>
<given-names>D.</given-names>
</name>
<name>
<surname>Korhonen</surname>
<given-names>L.</given-names>
</name>
<name>
<surname>Eriksson</surname>
<given-names>O.</given-names>
</name>
<name>
<surname>K&#xf5;ks</surname>
<given-names>S.</given-names>
</name>
</person-group> (<year>2017</year>). <article-title>Recent insights into the role of unfolded protein response in ER stress in Health and disease</article-title>. <source>Front. Cell Dev. Biol.</source> <volume>5</volume>, <fpage>48</fpage>. <pub-id pub-id-type="doi">10.3389/fcell.2017.00048</pub-id>
</citation>
</ref>
<ref id="B44">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Linna</surname>
<given-names>Z.</given-names>
</name>
<name>
<surname>Lifeng</surname>
<given-names>Z.</given-names>
</name>
</person-group> (<year>2017</year>). <article-title>Pioglitazone attenuates the effect of insulin resistance on carotid atherosclerosis in patients with type 2 diabetes mellitus</article-title>. <source>J. Clin. Ration. Drug Use</source> <volume>10</volume> (<issue>36</issue>), <fpage>47</fpage>&#x2013;<lpage>48</lpage>. <pub-id pub-id-type="doi">10.15887/j.cnki.13-1389/r.2017.36.023</pub-id>
</citation>
</ref>
<ref id="B45">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Liu</surname>
<given-names>M. Q.</given-names>
</name>
<name>
<surname>Chen</surname>
<given-names>Z.</given-names>
</name>
<name>
<surname>Chen</surname>
<given-names>L. X.</given-names>
</name>
</person-group> (<year>2016</year>). <article-title>Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases</article-title>. <source>Acta Pharmacol. Sin.</source> <volume>37</volume> (<issue>4</issue>), <fpage>425</fpage>&#x2013;<lpage>443</lpage>. <pub-id pub-id-type="doi">10.1038/aps.2015.145</pub-id>
</citation>
</ref>
<ref id="B46">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Liu</surname>
<given-names>X.</given-names>
</name>
<name>
<surname>Hou</surname>
<given-names>D.</given-names>
</name>
<name>
<surname>Lin</surname>
<given-names>F.</given-names>
</name>
<name>
<surname>Luo</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Xie</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Wang</surname>
<given-names>Y.</given-names>
</name>
<etal/>
</person-group> (<year>2019</year>). <article-title>The role of neurovascular unit damage in the occurrence and development of Alzheimer&#x2019;s disease</article-title>. <source>Rev. Neurosci.</source> <volume>30</volume> (<issue>5</issue>), <fpage>477</fpage>&#x2013;<lpage>484</lpage>. <pub-id pub-id-type="doi">10.1515/revneuro-2018-0056</pub-id>
</citation>
</ref>
<ref id="B47">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Lubrano</surname>
<given-names>V.</given-names>
</name>
<name>
<surname>Balzan</surname>
<given-names>S.</given-names>
</name>
</person-group> (<year>2014</year>). <article-title>LOX-1 and ROS, inseparable factors in the process of endothelial damage</article-title>. <source>Free Radic. Res.</source> <volume>48</volume> (<issue>8</issue>), <fpage>841</fpage>&#x2013;<lpage>848</lpage>. <pub-id pub-id-type="doi">10.3109/10715762.2014.929122</pub-id>
</citation>
</ref>
<ref id="B48">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Matthews</surname>
<given-names>K. A.</given-names>
</name>
<name>
<surname>Xu</surname>
<given-names>W.</given-names>
</name>
<name>
<surname>Gaglioti</surname>
<given-names>A. H.</given-names>
</name>
<name>
<surname>Holt</surname>
<given-names>J. B.</given-names>
</name>
<name>
<surname>Croft</surname>
<given-names>J. B.</given-names>
</name>
<name>
<surname>Mack</surname>
<given-names>D.</given-names>
</name>
<etal/>
</person-group> (<year>2019</year>). <article-title>Racial and ethnic estimates of Alzheimer&#x2019;s disease and related dementias in the United States (2015-2060) in adults aged &#x2265;65 years</article-title>. <source>Alzheimers Dement.</source> <volume>15</volume> (<issue>1</issue>), <fpage>17</fpage>&#x2013;<lpage>24</lpage>. <pub-id pub-id-type="doi">10.1016/j.jalz.2018.06.3063</pub-id>
</citation>
</ref>
<ref id="B49">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Milutinovi&#x107;</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>&#x160;uput</surname>
<given-names>D.</given-names>
</name>
<name>
<surname>Zorc-Pleskovi&#x10d;</surname>
<given-names>R.</given-names>
</name>
</person-group> (<year>2020</year>). <article-title>Pathogenesis of atherosclerosis in the tunica intima, media, and adventitia of coronary arteries: an updated review</article-title>. <source>Bosn. J. Basic Med. Sci.</source> <volume>20</volume> (<issue>1</issue>), <fpage>21</fpage>&#x2013;<lpage>30</lpage>. <pub-id pub-id-type="doi">10.17305/bjbms.2019.4320</pub-id>
</citation>
</ref>
<ref id="B50">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Moore</surname>
<given-names>K. J.</given-names>
</name>
<name>
<surname>Tabas</surname>
<given-names>I.</given-names>
</name>
</person-group> (<year>2011</year>). <article-title>Macrophages in the pathogenesis of atherosclerosis</article-title>. <source>Cell</source> <volume>145</volume> (<issue>3</issue>), <fpage>341</fpage>&#x2013;<lpage>355</lpage>. <pub-id pub-id-type="doi">10.1016/j.cell.2011.04.005</pub-id>
</citation>
</ref>
<ref id="B51">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Myoishi</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Hao</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Minamino</surname>
<given-names>T.</given-names>
</name>
<name>
<surname>Watanabe</surname>
<given-names>K.</given-names>
</name>
<name>
<surname>Nishihira</surname>
<given-names>K.</given-names>
</name>
<name>
<surname>Hatakeyama</surname>
<given-names>K.</given-names>
</name>
<etal/>
</person-group> (<year>2007</year>). <article-title>Increased endoplasmic reticulum stress in atherosclerotic plaques associated with acute coronary syndrome</article-title>. <source>Circulation</source> <volume>116</volume> (<issue>11</issue>), <fpage>1226</fpage>&#x2013;<lpage>1233</lpage>. <pub-id pub-id-type="doi">10.1161/CIRCULATIONAHA.106.682054</pub-id>
</citation>
</ref>
<ref id="B52">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Nebel</surname>
<given-names>R. A.</given-names>
</name>
<name>
<surname>Aggarwal</surname>
<given-names>N. T.</given-names>
</name>
<name>
<surname>Barnes</surname>
<given-names>L. L.</given-names>
</name>
<name>
<surname>Gallagher</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Goldstein</surname>
<given-names>J. M.</given-names>
</name>
<name>
<surname>Kantarci</surname>
<given-names>K.</given-names>
</name>
<etal/>
</person-group> (<year>2018</year>). <article-title>Understanding the impact of sex and gender in Alzheimer&#x2019;s disease: a call to action</article-title>. <source>Alzheimers Dement.</source> <volume>14</volume> (<issue>9</issue>), <fpage>1171</fpage>&#x2013;<lpage>1183</lpage>. <pub-id pub-id-type="doi">10.1016/j.jalz.2018.04.008</pub-id>
</citation>
</ref>
<ref id="B53">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Oakes</surname>
<given-names>S. A.</given-names>
</name>
<name>
<surname>Papa</surname>
<given-names>F. R.</given-names>
</name>
</person-group> (<year>2015</year>). <article-title>The role of endoplasmic reticulum stress in human pathology</article-title>. <source>Annu. Rev. Pathol.</source> <volume>10</volume>, <fpage>173</fpage>&#x2013;<lpage>194</lpage>. <pub-id pub-id-type="doi">10.1146/annurev-pathol-012513-104649</pub-id>
</citation>
</ref>
<ref id="B54">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Oh</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Riek</surname>
<given-names>A. E.</given-names>
</name>
<name>
<surname>Weng</surname>
<given-names>S.</given-names>
</name>
<name>
<surname>Petty</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Kim</surname>
<given-names>D.</given-names>
</name>
<name>
<surname>Colonna</surname>
<given-names>M.</given-names>
</name>
<etal/>
</person-group> (<year>2012</year>). <article-title>Endoplasmic reticulum stress controls M2 macrophage differentiation and foam cell formation</article-title>. <source>J. Biol. Chem.</source> <volume>287</volume> (<issue>15</issue>), <fpage>11629</fpage>&#x2013;<lpage>11641</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.M111.338673</pub-id>
</citation>
</ref>
<ref id="B74">
<citation citation-type="book">
<person-group person-group-type="author">
<name>
<surname>Organization</surname>
<given-names>W. H.</given-names>
</name>
</person-group> (<year>2011</year>). <source>Who web site on cardiovascular diseases: strategic priorities, fact sheets, world health day 2013, publications</source>.</citation>
</ref>
<ref id="B55">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Pisto</surname>
<given-names>P.</given-names>
</name>
<name>
<surname>Santaniemi</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Bloigu</surname>
<given-names>R.</given-names>
</name>
<name>
<surname>Ukkola</surname>
<given-names>O.</given-names>
</name>
<name>
<surname>Kes&#xe4;niemi</surname>
<given-names>Y. A.</given-names>
</name>
</person-group> (<year>2014</year>). <article-title>Fatty liver predicts the risk for cardiovascular events in middle-aged population: a population-based cohort study</article-title>. <source>BMJ Open</source> <volume>4</volume> (<issue>3</issue>), <fpage>e004973</fpage>. <pub-id pub-id-type="doi">10.1136/bmjopen-2014-004973</pub-id>
</citation>
</ref>
<ref id="B56">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Ren</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Bi</surname>
<given-names>Y.</given-names>
</name>
<name>
<surname>Sowers</surname>
<given-names>J. R.</given-names>
</name>
<name>
<surname>Hetz</surname>
<given-names>C.</given-names>
</name>
<name>
<surname>Zhang</surname>
<given-names>Y.</given-names>
</name>
</person-group> (<year>2021</year>). <article-title>Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases</article-title>. <source>Nat. Rev. Cardiol.</source> <volume>18</volume> (<issue>7</issue>), <fpage>499</fpage>&#x2013;<lpage>521</lpage>. <pub-id pub-id-type="doi">10.1038/s41569-021-00511-w</pub-id>
</citation>
</ref>
<ref id="B57">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Ron</surname>
<given-names>D.</given-names>
</name>
<name>
<surname>Walter</surname>
<given-names>P.</given-names>
</name>
</person-group> (<year>2007</year>). <article-title>Signal integration in the endoplasmic reticulum unfolded protein response</article-title>. <source>Nat. Rev. Mol. Cell Biol.</source> <volume>8</volume> (<issue>7</issue>), <fpage>519</fpage>&#x2013;<lpage>529</lpage>. <pub-id pub-id-type="doi">10.1038/nrm2199</pub-id>
</citation>
</ref>
<ref id="B58">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Rondanelli</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Perna</surname>
<given-names>S.</given-names>
</name>
<name>
<surname>Peroni</surname>
<given-names>G.</given-names>
</name>
<name>
<surname>Guido</surname>
<given-names>D.</given-names>
</name>
</person-group> (<year>2016</year>). <article-title>A bibliometric study of scientific literature in Scopus on botanicals for treatment of androgenetic alopecia</article-title>. <source>J. Cosmet. Dermatol</source> <volume>15</volume> (<issue>2</issue>), <fpage>120</fpage>&#x2013;<lpage>130</lpage>. <pub-id pub-id-type="doi">10.1111/jocd.12198</pub-id>
</citation>
</ref>
<ref id="B59">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Salminen</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Kaarniranta</surname>
<given-names>K.</given-names>
</name>
<name>
<surname>Kauppinen</surname>
<given-names>A.</given-names>
</name>
</person-group> (<year>2020</year>). <article-title>ER stress activates immunosuppressive network: implications for aging and Alzheimer&#x2019;s disease</article-title>. <source>J. Mol. Med. Berl.</source> <volume>98</volume> (<issue>5</issue>), <fpage>633</fpage>&#x2013;<lpage>650</lpage>. <pub-id pub-id-type="doi">10.1007/s00109-020-01904-z</pub-id>
</citation>
</ref>
<ref id="B60">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Schmitz</surname>
<given-names>M. L.</given-names>
</name>
<name>
<surname>Shaban</surname>
<given-names>M. S.</given-names>
</name>
<name>
<surname>Albert</surname>
<given-names>B. V.</given-names>
</name>
<name>
<surname>G&#xf6;k&#xe7;en</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Kracht</surname>
<given-names>M.</given-names>
</name>
</person-group> (<year>2018</year>). <article-title>The crosstalk of endoplasmic reticulum (ER) stress pathways with NF-&#x3ba;B: complex mechanisms relevant for cancer, inflammation and infection</article-title>. <source>Biomedicines</source> <volume>6</volume> (<issue>2</issue>), <fpage>58</fpage>. <pub-id pub-id-type="doi">10.3390/biomedicines6020058</pub-id>
</citation>
</ref>
<ref id="B61">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Shio</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Haley</surname>
<given-names>N. J.</given-names>
</name>
<name>
<surname>Fowler</surname>
<given-names>S.</given-names>
</name>
</person-group> (<year>1979</year>). <article-title>Characterization of lipid-laden aortic cells from cholesterol-fed rabbits. III. Intracellular localization of cholesterol and cholesteryl ester</article-title>. <source>Lab. Invest.</source> <volume>41</volume> (<issue>2</issue>), <fpage>160</fpage>&#x2013;<lpage>167</lpage>.</citation>
</ref>
<ref id="B62">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Small</surname>
<given-names>D. M.</given-names>
</name>
<name>
<surname>Bond</surname>
<given-names>M. G.</given-names>
</name>
<name>
<surname>Waugh</surname>
<given-names>D.</given-names>
</name>
<name>
<surname>Prack</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Sawyer</surname>
<given-names>J. K.</given-names>
</name>
</person-group> (<year>1984</year>). <article-title>Physicochemical and histological changes in the arterial wall of nonhuman primates during progression and regression of atherosclerosis</article-title>. <source>J. Clin. Invest.</source> <volume>73</volume> (<issue>6</issue>), <fpage>1590</fpage>&#x2013;<lpage>1605</lpage>. <pub-id pub-id-type="doi">10.1172/JCI111366</pub-id>
</citation>
</ref>
<ref id="B63">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Suzuki</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Kurihara</surname>
<given-names>Y.</given-names>
</name>
<name>
<surname>Takeya</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Kamada</surname>
<given-names>N.</given-names>
</name>
<name>
<surname>Kataoka</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Jishage</surname>
<given-names>K.</given-names>
</name>
<etal/>
</person-group> (<year>1997</year>). <article-title>A role for macrophage scavenger receptors in atherosclerosis and susceptibility to infection</article-title>. <source>Nature</source> <volume>386</volume> (<issue>6622</issue>), <fpage>292</fpage>&#x2013;<lpage>296</lpage>. <pub-id pub-id-type="doi">10.1038/386292a0</pub-id>
</citation>
</ref>
<ref id="B64">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Tabas</surname>
<given-names>I.</given-names>
</name>
</person-group> (<year>2000</year>). <article-title>Cholesterol and phospholipid metabolism in macrophages</article-title>. <source>Biochim. Biophys. Acta</source> <volume>1529</volume> (<issue>1-3</issue>), <fpage>164</fpage>&#x2013;<lpage>174</lpage>. <pub-id pub-id-type="doi">10.1016/s1388-1981(00)00146-3</pub-id>
</citation>
</ref>
<ref id="B65">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Tabas</surname>
<given-names>I.</given-names>
</name>
</person-group> (<year>2005</year>). <article-title>Consequences and therapeutic implications of macrophage apoptosis in atherosclerosis: the importance of lesion stage and phagocytic efficiency</article-title>. <source>Arterioscler. Thromb. Vasc. Biol.</source> <volume>25</volume> (<issue>11</issue>), <fpage>2255</fpage>&#x2013;<lpage>2264</lpage>. <pub-id pub-id-type="doi">10.1161/01.ATV.0000184783.04864.9f</pub-id>
</citation>
</ref>
<ref id="B66">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Tabas</surname>
<given-names>I.</given-names>
</name>
</person-group> (<year>2010</year>). <article-title>The role of endoplasmic reticulum stress in the progression of atherosclerosis</article-title>. <source>Circ. Res.</source> <volume>107</volume> (<issue>7</issue>), <fpage>839</fpage>&#x2013;<lpage>850</lpage>. <pub-id pub-id-type="doi">10.1161/CIRCRESAHA.110.224766</pub-id>
</citation>
</ref>
<ref id="B67">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Tabas</surname>
<given-names>I.</given-names>
</name>
<name>
<surname>Ron</surname>
<given-names>D.</given-names>
</name>
</person-group> (<year>2011</year>). <article-title>Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress</article-title>. <source>Nat. Cell Biol.</source> <volume>13</volume> (<issue>3</issue>), <fpage>184</fpage>&#x2013;<lpage>190</lpage>. <pub-id pub-id-type="doi">10.1038/ncb0311-184</pub-id>
</citation>
</ref>
<ref id="B68">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Takousis</surname>
<given-names>P.</given-names>
</name>
<name>
<surname>Sadlon</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Schulz</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Wohlers</surname>
<given-names>I.</given-names>
</name>
<name>
<surname>Dobricic</surname>
<given-names>V.</given-names>
</name>
<name>
<surname>Middleton</surname>
<given-names>L.</given-names>
</name>
<etal/>
</person-group> (<year>2019</year>). <article-title>Differential expression of microRNAs in Alzheimer&#x2019;s disease brain, blood, and cerebrospinal fluid</article-title>. <source>Alzheimers Dement.</source> <volume>15</volume> (<issue>11</issue>), <fpage>1468</fpage>&#x2013;<lpage>1477</lpage>. <pub-id pub-id-type="doi">10.1016/j.jalz.2019.06.4952</pub-id>
</citation>
</ref>
<ref id="B69">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Targher</surname>
<given-names>G.</given-names>
</name>
<name>
<surname>Byrne</surname>
<given-names>C. D.</given-names>
</name>
<name>
<surname>Lonardo</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Zoppini</surname>
<given-names>G.</given-names>
</name>
<name>
<surname>Barbui</surname>
<given-names>C.</given-names>
</name>
</person-group> (<year>2016</year>). <article-title>Non-alcoholic fatty liver disease and risk of incident cardiovascular disease: a meta-analysis</article-title>. <source>J. Hepatol.</source> <volume>65</volume> (<issue>3</issue>), <fpage>589</fpage>&#x2013;<lpage>600</lpage>. <pub-id pub-id-type="doi">10.1016/j.jhep.2016.05.013</pub-id>
</citation>
</ref>
<ref id="B70">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Thorp</surname>
<given-names>E.</given-names>
</name>
<name>
<surname>Li</surname>
<given-names>G.</given-names>
</name>
<name>
<surname>Seimon</surname>
<given-names>T. A.</given-names>
</name>
<name>
<surname>Kuriakose</surname>
<given-names>G.</given-names>
</name>
<name>
<surname>Ron</surname>
<given-names>D.</given-names>
</name>
<name>
<surname>Tabas</surname>
<given-names>I.</given-names>
</name>
</person-group> (<year>2009</year>). <article-title>Reduced apoptosis and plaque necrosis in advanced atherosclerotic lesions of Apoe-/- and Ldlr-/- mice lacking CHOP</article-title>. <source>Cell Metab.</source> <volume>9</volume> (<issue>5</issue>), <fpage>474</fpage>&#x2013;<lpage>481</lpage>. <pub-id pub-id-type="doi">10.1016/j.cmet.2009.03.003</pub-id>
</citation>
</ref>
<ref id="B71">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Tian</surname>
<given-names>S.</given-names>
</name>
<name>
<surname>Li</surname>
<given-names>B.</given-names>
</name>
<name>
<surname>Lei</surname>
<given-names>P.</given-names>
</name>
<name>
<surname>Yang</surname>
<given-names>X.</given-names>
</name>
<name>
<surname>Zhang</surname>
<given-names>X.</given-names>
</name>
<name>
<surname>Bao</surname>
<given-names>Y.</given-names>
</name>
<etal/>
</person-group> (<year>2018</year>). <article-title>Sulforaphane improves abnormal lipid metabolism via both ERS-dependent XBP1/ACC &#x26;SCD1 and ERS-independent SREBP/FAS pathways</article-title>. <source>Mol. Nutr. Food Res.</source> <volume>62</volume> (<issue>6</issue>), <fpage>e1700737</fpage>. <pub-id pub-id-type="doi">10.1002/mnfr.201700737</pub-id>
</citation>
</ref>
<ref id="B72">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Toyomasu</surname>
<given-names>K.</given-names>
</name>
<name>
<surname>Adachi</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Enomoto</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Fukami</surname>
<given-names>A.</given-names>
</name>
<name>
<surname>Nakamura</surname>
<given-names>S.</given-names>
</name>
<name>
<surname>Nohara</surname>
<given-names>Y.</given-names>
</name>
<etal/>
</person-group> (<year>2021</year>). <article-title>Impact of combined elevations of homocysteine and asymmetric dimethylarginine on all-cause death - the Tanushimaru Study</article-title>. <source>J. Cardiol.</source> <volume>78</volume> (<issue>2</issue>), <fpage>129</fpage>&#x2013;<lpage>135</lpage>. <pub-id pub-id-type="doi">10.1016/j.jjcc.2021.01.011</pub-id>
</citation>
</ref>
<ref id="B73">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>van Eck</surname>
<given-names>N. J.</given-names>
</name>
<name>
<surname>Waltman</surname>
<given-names>L.</given-names>
</name>
</person-group> (<year>2010</year>). <article-title>Software survey: VOSviewer, a computer program for bibliometric mapping</article-title>. <source>Scientometrics</source> <volume>84</volume> (<issue>2</issue>), <fpage>523</fpage>&#x2013;<lpage>538</lpage>. <pub-id pub-id-type="doi">10.1007/s11192-009-0146-3</pub-id>
</citation>
</ref>
<ref id="B75">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Wu</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Chen</surname>
<given-names>Z.</given-names>
</name>
<name>
<surname>Chen</surname>
<given-names>J. Z.</given-names>
</name>
<name>
<surname>Pei</surname>
<given-names>L. G.</given-names>
</name>
<name>
<surname>Xie</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Wei</surname>
<given-names>Z. H.</given-names>
</name>
<etal/>
</person-group> (<year>2018</year>). <article-title>High mobility group B-1 (HMGB-1) promotes apoptosis of macrophage-derived foam cells by inducing endoplasmic reticulum stress</article-title>. <source>Cell Physiol. Biochem.</source> <volume>48</volume> (<issue>3</issue>), <fpage>1019</fpage>&#x2013;<lpage>1029</lpage>. <pub-id pub-id-type="doi">10.1159/000491970</pub-id>
</citation>
</ref>
<ref id="B76">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Yan</surname>
<given-names>L.</given-names>
</name>
</person-group> (<year>2005</year>). <article-title>Inflammation, insulin resistance common to type 2 diabetes and atherosclerosis</article-title>. <source>Foreign Med. Endocrinol.</source> (<issue>03</issue>), <fpage>150</fpage>&#x2013;<lpage>152</lpage>.</citation>
</ref>
<ref id="B77">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Yang</surname>
<given-names>S.</given-names>
</name>
<name>
<surname>Wu</surname>
<given-names>M.</given-names>
</name>
<name>
<surname>Li</surname>
<given-names>X.</given-names>
</name>
<name>
<surname>Zhao</surname>
<given-names>R.</given-names>
</name>
<name>
<surname>Zhao</surname>
<given-names>Y.</given-names>
</name>
<name>
<surname>Liu</surname>
<given-names>L.</given-names>
</name>
<etal/>
</person-group> (<year>2020</year>). <article-title>Role of endoplasmic reticulum stress in atherosclerosis and its potential as a therapeutic target</article-title>. <source>Oxid. Med. Cell Longev.</source> <volume>2020</volume>, <fpage>9270107</fpage>. <pub-id pub-id-type="doi">10.1155/2020/9270107</pub-id>
</citation>
</ref>
<ref id="B78">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Yao</surname>
<given-names>S.</given-names>
</name>
<name>
<surname>Miao</surname>
<given-names>C.</given-names>
</name>
<name>
<surname>Tian</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Sang</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Yang</surname>
<given-names>N.</given-names>
</name>
<name>
<surname>Jiao</surname>
<given-names>P.</given-names>
</name>
<etal/>
</person-group> (<year>2014a</year>). <article-title>Endoplasmic reticulum stress promotes macrophage-derived foam cell formation by up-regulating cluster of differentiation 36 (CD36) expression</article-title>. <source>J. Biol. Chem.</source> <volume>289</volume> (<issue>7</issue>), <fpage>4032</fpage>&#x2013;<lpage>4042</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.M113.524512</pub-id>
</citation>
</ref>
<ref id="B79">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Yao</surname>
<given-names>S.</given-names>
</name>
<name>
<surname>Yang</surname>
<given-names>N.</given-names>
</name>
<name>
<surname>Song</surname>
<given-names>G.</given-names>
</name>
<name>
<surname>Sang</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Tian</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Miao</surname>
<given-names>C.</given-names>
</name>
<etal/>
</person-group> (<year>2012</year>). <article-title>Minimally modified low-density lipoprotein induces macrophage endoplasmic reticulum stress via toll-like receptor 4</article-title>. <source>Biochim. Biophys. Acta</source> <volume>1821</volume> (<issue>7</issue>), <fpage>954</fpage>&#x2013;<lpage>963</lpage>. <pub-id pub-id-type="doi">10.1016/j.bbalip.2012.03.003</pub-id>
</citation>
</ref>
<ref id="B80">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Yao</surname>
<given-names>S. T.</given-names>
</name>
<name>
<surname>Zhao</surname>
<given-names>L.</given-names>
</name>
<name>
<surname>Miao</surname>
<given-names>C.</given-names>
</name>
<name>
<surname>Tian</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Yang</surname>
<given-names>N. N.</given-names>
</name>
<name>
<surname>Guo</surname>
<given-names>S. D.</given-names>
</name>
<etal/>
</person-group> (<year>2014b</year>). <article-title>Endoplasmic reticulum stress mediates oxidized low density lipoprotein-induced scavenger receptor A1 upregulation in macrophages</article-title>. <source>Sheng Li Xue Bao</source> <volume>66</volume> (<issue>5</issue>), <fpage>612</fpage>&#x2013;<lpage>618</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.M113.524512</pub-id>
</citation>
</ref>
<ref id="B81">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Yue</surname>
<given-names>C.</given-names>
</name>
<name>
<surname>Chao-mei</surname>
<given-names>C.</given-names>
</name>
<name>
<surname>Ze-yuan</surname>
<given-names>L.</given-names>
</name>
<name>
<surname>Zhi-gang</surname>
<given-names>H.</given-names>
</name>
<name>
<surname>Xian-wen</surname>
<given-names>W.</given-names>
</name>
</person-group> (<year>2015</year>). <article-title>The methodology function of Cite Space mapping knowledge domains</article-title>. <source>Sci. Res.</source> <volume>33</volume> (<issue>02</issue>), <fpage>242</fpage>&#x2013;<lpage>253</lpage>. <pub-id pub-id-type="doi">10.16192/j.cnki.1003-2053.2015.02.009</pub-id>
</citation>
</ref>
<ref id="B82">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Zhou</surname>
<given-names>J.</given-names>
</name>
<name>
<surname>Lhot&#xe1;k</surname>
<given-names>S.</given-names>
</name>
<name>
<surname>Hilditch</surname>
<given-names>B. A.</given-names>
</name>
<name>
<surname>Austin</surname>
<given-names>R. C.</given-names>
</name>
</person-group> (<year>2005</year>). <article-title>Activation of the unfolded protein response occurs at all stages of atherosclerotic lesion development in apolipoprotein E-deficient mice</article-title>. <source>Circulation</source> <volume>111</volume> (<issue>14</issue>), <fpage>1814</fpage>&#x2013;<lpage>1821</lpage>. <pub-id pub-id-type="doi">10.1161/01.CIR.0000160864.31351.C1</pub-id>
</citation>
</ref>
<ref id="B83">
<citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname>Zhu</surname>
<given-names>G.</given-names>
</name>
<name>
<surname>Lee</surname>
<given-names>A. S.</given-names>
</name>
</person-group> (<year>2015</year>). <article-title>Role of the unfolded protein response, GRP78 and GRP94 in organ homeostasis</article-title>. <source>J. Cell Physiol.</source> <volume>230</volume> (<issue>7</issue>), <fpage>1413</fpage>&#x2013;<lpage>1420</lpage>. <pub-id pub-id-type="doi">10.1002/jcp.24923</pub-id>
</citation>
</ref>
</ref-list>
</back>
</article>