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<front>
<journal-meta>
<journal-id journal-id-type="publisher-id">Front. Immunol.</journal-id>
<journal-title>Frontiers in Immunology</journal-title>
<abbrev-journal-title abbrev-type="pubmed">Front. Immunol.</abbrev-journal-title>
<issn pub-type="epub">1664-3224</issn>
<publisher>
<publisher-name>Frontiers Media S.A.</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="doi">10.3389/fimmu.2022.1085875</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Immunology</subject>
<subj-group>
<subject>Editorial</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group>
<article-title>Editorial: Clinical management, pathogenesis and biomarkers of cardiovascular disease associated with systemic autoimmune disorders</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Perez-Sanchez</surname>
<given-names>Carlos</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
<xref ref-type="author-notes" rid="fn001">
<sup>*</sup>
</xref>
<uri xlink:href="https://loop.frontiersin.org/people/713530"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Pineda-Torra</surname>
<given-names>In&#xe9;s</given-names>
</name>
<xref ref-type="aff" rid="aff4">
<sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Lopez-Pedrera</surname>
<given-names>Chary</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
<uri xlink:href="https://loop.frontiersin.org/people/575576"/>
</contrib>
</contrib-group>
<aff id="aff1">
<sup>1</sup>
<institution>Maimonides Biomedical Research Institute of Cordoba (IMIBIC)</institution>, <addr-line>Cordoba</addr-line>, <country>Spain</country>
</aff>
<aff id="aff2">
<sup>2</sup>
<institution>University of Cordoba</institution>, <addr-line>Cordoba</addr-line>, <country>Spain</country>
</aff>
<aff id="aff3">
<sup>3</sup>
<institution>Hospital Universitario Reina Sof&#xed;a</institution>, <addr-line>Cordoba</addr-line>, <country>Spain</country>
</aff>
<aff id="aff4">
<sup>4</sup>
<institution>Andalusian Center of Molecular Biology and Regenerative Medicine, Spanish National Research Council (CSIC)</institution>, <addr-line>Seville</addr-line>, <country>Spain</country>
</aff>
<author-notes>
<fn fn-type="edited-by">
<p>Edited and Reviewed by: Betty Diamond, Feinstein Institute for Medical Research, United States</p>
</fn>
<fn fn-type="corresp" id="fn001">
<p>*Correspondence: Carlos Perez-Sanchez, <email xlink:href="mailto:b32pesac@uco.es">b32pesac@uco.es</email>
</p>
</fn>
<fn fn-type="other" id="fn002">
<p>This article was submitted to Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders, a section of the journal Frontiers in Immunology</p>
</fn>
</author-notes>
<pub-date pub-type="epub">
<day>23</day>
<month>11</month>
<year>2022</year>
</pub-date>
<pub-date pub-type="collection">
<year>2022</year>
</pub-date>
<volume>13</volume>
<elocation-id>1085875</elocation-id>
<history>
<date date-type="received">
<day>31</day>
<month>10</month>
<year>2022</year>
</date>
<date date-type="accepted">
<day>10</day>
<month>11</month>
<year>2022</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright &#xa9; 2022 Perez-Sanchez, Pineda-Torra and Lopez-Pedrera</copyright-statement>
<copyright-year>2022</copyright-year>
<copyright-holder>Perez-Sanchez, Pineda-Torra and Lopez-Pedrera</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>
<related-article id="RA1" related-article-type="commentary-article" xlink:href="https://www.frontiersin.org/research-topics/25119#articles" ext-link-type="uri">Editorial on the Research Topic <article-title>Clinical management, pathogenesis and biomarkers of cardiovascular disease associated with systemic autoimmune disorders</article-title>
</related-article>
<kwd-group>
<kwd>cardiovascular disease</kwd>
<kwd>autoimmune disease</kwd>
<kwd>inflammatory disease</kwd>
<kwd>biomarker</kwd>
<kwd>pathogenesis</kwd>
</kwd-group>
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<word-count count="951"/>
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</front>
<body>
<p>In this Research Topic several studies have analysed the clinical and molecular profile related to cardiovascular disease (CVD) development in a range of inflammatory and systemic autoimmune diseases, including systemic lupus erythematosus (SLE), psoriatic arthritis, rheumatoid arthritis and spondylarthritis among others. Novel molecular mechanisms and biomarkers have been characterized along with clinical tools and approaches to manage this prevalent comorbidity.</p>
<p>In the case of SLE, three studies have explored at the molecular level the underlaying mechanisms associated with CVD. <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fimmu.2022.827355">Quevedo-Abeledo et&#xa0;al.</ext-link>, studied the levels of three CVD molecules involved in the metabolism of triglycerides, such as lipoprotein lipase (LPL), angiopoietin-like protein 4 (ANGPLT4), and apolipoprotein C-III (ApoC3), in 185 patients with SLE and 162 healthy donors. Performing a multivariable analysis, they identified that the LPL, ANGPLT4 and ApoC3, axis is altered in SLE and associated with the disease damage score. <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fimmu.2022.935545">Wang et&#xa0;al.</ext-link>, used public transcriptomic data to gain insight into the involvement of new players and pathways related to the development of atherosclerosis in SLE patients. They identified 5 hub genes (SIGLEC1, CD163, CCR1, MMP9, and IL1RN) which might promote the monocytes differentiation into macrophages and the pathway of IL-17 signalling as potential mechanisms involved in the atherosclerotic process of SLE patients. <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fimmu.2022.974826">Guzman-Martinez et&#xa0;al.</ext-link>, reviewed the association of the immune system with the pathogenesis of endothelial damage and atherosclerosis in SLE patients, including inflammatory mediators, specific circulating cell populations and autoantibodies. Additionally, they discussed the utility of the immune system as early CVD biomarkers and therapeutic targets in SLE.</p>
<p>On the other hand, <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fimmu.2022.894171">Remuzgo-Mart&#xed;nez et&#xa0;al.</ext-link>, analysed the role of the protein irisin as a serological and genetic biomarker of CV risk, disease severity and subclinical atherosclerosis in a cohort of 725 patients with axial spondylarthritis (axSpA). Their results suggested that low levels of irisin in the serum could be considered a marker of high CV risk, more severe disease and the presence of subclinical atherosclerosis, in axSpA patients. Furthermore, they found that irisin may also constitute a biomarker of disease activity in axSpA at the genetic level.</p>
<p>In the case of inflammatory arthritis like rheumatoid arthritis (RA) and psoriatic arthritis (PsA), <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fimmu.2022.997270">Barbarroja et&#xa0;al.</ext-link>, reviewed the interplay of hepatic alterations and CVD, analysing different mechanisms where autoimmunity, chronic inflammation, metabolic deregulation and treatments seem to have an key role. They also discussed the latest controversies regarding the effects of anti-inflammatory therapies used in PsA and RA in the liver damage, such as biologics and DMARDs such as, leflunomide or methotrexate. <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fimmu.2022.909760">Schwartz et&#xa0;al.</ext-link>, also analyzed in a cohort of PsA patients, the associations of metabolic dysregulation and systemic inflammation with coronary artery disease (CAD) measuring traditional CVD risk factors, serum markers of metabolic dysfunction, inflammatory cytokines and inflammation in specific tissues by using positron emission tomography-computed tomography (PET-CT). They identified metabolic and inflammatory players associated with subclinical CAD in PsA, including inflammation in adipose tissue which might be considered as novel target for CVD prevention and treatment in PsA.</p>
<p>The association between Psoriasis and the risk of CVD was also explored by <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fimmu.2022.918224">Gao et al.</ext-link>, using mendelian randomization and genome-wide association study (GWAS). The analysis suggested a potential causal link between CVD and psoriasis.</p>
<p>Lastly, two studies in this issue evaluated the CV involvement in rare systemic autoimmune disorders.</p>
<p>
<ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fimmu.2022.928861">Zhou et&#xa0;al.</ext-link>, analyzed in anti-melanoma differentiation-associated gene 5 (anti-MDA5) antibody-positive dermatomyositis (DM)//clinically amyopathic dermatomyositis (anti-MDA5 Ab+ DM/CADM) the myocardial involvement. Anti-MDA5 dermatomyositis is a rare autoimmune disease, with high prevalence in Japanese patients with clinically amyopathic dermatomyositis and progressive interstitial lung disease. It also shows systemic manifestations affecting skeletal muscle, skin, and other organs.</p>
<p>In a cohort of seventy-six hospitalized patients suffering this disorder, this study identified twelve patients with MI (16%), associated with severe cardiovascular complications and adverse evolution of the disease. They concluded that myocardial involvement is an independent poor prognostic factor of patients with anti-MDA5 Ab+ DM/CADM.</p>
<p>
<ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fimmu.2022.828863">Huang et&#xa0;al.</ext-link>, investigated the efficacy of percutaneous transluminal pulmonary angioplasty (PTPA) in patients with Takayasu arteritis (TA) and pulmonary hypertension (PH) and pulmonary artery stenosis.</p>
<p>Takayasu&#x2019;s arteritis is a rare chronic inflammatory autoimmune condition that impact the largest blood vessels in the body (aorta) and its branches, the supra-aortic trunks.</p>
<p>Results of this study, analyzing 183 lesions from 79 surgeries carried out on 32 patients with TA and PH, indicated that PTPA improved clinical symptoms, hemodynamic parameters, and exercise tolerance, in patients with TA pulmonary artery stenosis and PH. Furthermore, reperfusion pulmonary edema was significantly reduced, and no patient died of PTPA-related complications with guidance from the pressure wire.</p>
<p>Overall, these findings might be important for healthcare resource planning and preventive approaches. These 9 articles substantial CV-risk observed in autoimmune diseases patients, suggests that strategies to reduce CV-risk should become a routine part of the management of autoimmune disease patients. However, the causes of cardiovascular involvement associated with systemic autoimmune diseases, and their potential therapy, require further research.</p>
<sec id="s1" sec-type="author-contributions">
<title>Author contributions</title>
<p>All authors listed have made a substantial, direct, and intellectual contribution to the work and approved it for publication.</p>
</sec>
<sec id="s2" sec-type="COI-statement">
<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 id="s3" sec-type="disclaimer">
<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>
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