Myocardial infarction (MI), a severe form of coronary heart disease (CHD), results from prolonged ischemia and hypoxia due to blocked coronary arteries, posing significant life-threatening risks. According to the World Health Organization (WHO), cardiovascular diseases remain the global leading cause of death, with CHD accounting for the largest proportion. According to statistics, approximately one million individuals in China experience acute myocardial infarctions annually, and the incidence rate is gradually increasing (Author Anonymous, 2021). Therefore, identifying new therapeutic targets for myocardial infarction is of paramount importance. Long non-coding RNAs (lncRNAs) are a class of non-coding RNA molecules longer than 200 nucleotides that do not encode proteins. These lncRNAs are widely implicated in vital cellular processes such as metabolism, signal transduction, proliferation, differentiation, apoptosis, and cell death, and are particularly relevant to the onset and progression of cardiovascular diseases (Jiao et al., 2019). In recent years, there has been a continuous increase in the number of publications related to lncRNAs, which remain a focal point of RNA functional studies.

Bibliometrics, an interdisciplinary field utilizing mathematical and statistical methods, effectively quantifies vast bodies of knowledge across various domains. This methodology excels in mapping research trends, analyzing contributions by countries, institutions, and authors, and identifying emerging topics within a scientific discipline. Unlike systematic reviews and meta-analyses, which synthesize findings from select studies to assess specific hypotheses, bibliometrics offers a broader overview, providing visualizations of data trends and network relationships. These capabilities make it particularly valuable for exploring extensive datasets and forecasting future research directions, thereby supporting the development of therapeutic policies and clinical guidelines. This study leverages bibliometric tools to delve into myocardial infarction-related lncRNA research, uncovering new insights and potential areas for further investigation.

To the best of our knowledge, this is the first comprehensive bibliometric analysis of literature concerning long non-coding RNAs (LncRNAs) associated with myocardial infarction (MI). This analysis aimed to assess research development over the past 23 years concerning MI-related lncRNAs. The literature from January 2000 to August 2023 has exhibited a continuous increasing trend, with an exponential growth pattern especially since 2018, publishing on average about 177.7 articles per year. This suggests increasing attention and interest in the potential role of lncRNAs in myocardial infarction, likely influenced by the high prevalence of cardiovascular diseases (Author Anonymous, 2021) and the pivotal role lncRNAs play in myocardial infarction (Ounzain et al., 2015; Zhang et al., 2016).

Secondly, China stands as the most productive country in the field, contributing 75.65% of the total publications. Although the United States and Germany produce fewer publications, their higher citation numbers suggest greater impact. Iran and Italy have also made notable contributions. International collaborations, especially between China and the United States, play a significant role, possibly due to varying levels of academic research support. Such international cooperation fosters interdisciplinary research and advances the field. Institutions like Harbin Medical University, Harvard University, and the University of California system have excelled in this research, indicating a stable scientific collaboration between institutions.

Additionally, an analysis of the publication years by institutions reveals that some organizations initiated their research at an early stage, while others have only recently begun to participate. Research on MI-related lncRNAs is chiefly disseminated across 445 journals within the realms of biology and medicine, with the top 10 journals accounting for 19% of the total publications. Circulation Research stands as the journal with the highest impact factor, underscoring the significance attributed to this area of study. The scope of this research encompasses multiple aspects including cardiovascular systems, cell biology, and physiology. Moreover, there is an interdisciplinary overlap with fields such as chemistry, applied physics, computer science, and statistics, highlighting the researchers’ quest to understand and harness the potential of MI-related lncRNAs across multiple disciplines. Such interdisciplinary research may offer novel perspectives and methodologies for the treatment and diagnosis of myocardial infarction.

Furthermore, key influential authors and hot keywords have been analyzed to identify renowned researchers, institutions, and key themes. For example, YAP KL’s work (Yap et al., 2010) on the interaction between Polycomb CBX7 and LncRNA-ANRIL has high citation counts, while VAUSORT M’s paper (Vausort et al., 2014) on peripheral blood lncRNA expression in acute myocardial infarction patients holds promise for prognostic applications. Research involving lncRNAs like MIAT, ANRIL, LincRNA-p21, and LIPCAR, among others, have gained considerable attention, revealing their diverse roles in vascular smooth muscle cell proliferation, apoptosis, and atherosclerosis. Authors such as Zhang et al. (2016), ZHANG L and LI Y have secured a prominent position in the research domain, as evidenced by their extensive publication records and high impact factors.

After myocardial infarction, the expression of lncRNAs changes significantly. Studies have shown that specific lncRNAs, such as ZFAS1 and CDR1AS, exhibit complementary changes following acute myocardial infarction, suggesting that these lncRNAs play important regulatory roles in cardiomyocyte injury and repair (Zhang et al., 2016). The expression levels of these lncRNAs can serve as biomarkers for myocardial infarction, aiding in the prediction of disease progression and patient prognosis. Several pivotal lncRNAs have garnered attention from researchers, such as MIAT, ANRIL, LincRNA-p21, LIPCAR, APF, CAIF. MIAT was identified in a large-scale case-control study (Ishii et al., 2006), and is a myocardial infarction susceptibility locus found on chromosome 22q12.1. MIAT regulates endothelial cell proliferation and apoptosis by acting as a ceRNA for miR-150, affecting VEGF expression and angiogenesis. MIAT also modulates inflammatory responses and oxidative stress, crucial in MI pathogenesis (Yan et al., 2015). ANRIL is located in the 9p21 genomic region, which also encodes cell cycle regulatory factors such as p14 (ARF), p15 (INK4b), and p16 (INK4a), potentially increasing the risk for clinical/subclinical coronary artery disease and aortic disease (Holdt et al., 2010). Further research suggests that ANRIL may modulate vascular smooth muscle cell proliferation, cell adhesion, and apoptosis through multiple mechanisms including cis, trans, and Polycomb complex protein binding, possibly contributing to the risk of coronary artery disease (Kotake et al., 2011; Pasmant et al., 2011; Congrains et al., 2012a; Congrains et al., 2012b; Motterle et al., 2012; Tsai et al., 2012; Ahmed et al., 2013; Bochenek et al., 2013; Holdt et al., 2013; Johnson et al., 2013; Chen et al., 2014). ANRIL interacts with PRC1 and PRC2 to repress CDKN2A/B, promoting VSMC proliferation and inhibiting apoptosis (Yap et al., 2010). ANRIL also regulates inflammatory gene expression and cellular senescence, contributing to atherosclerosis and CAD (Holdt et al., 2010; Congrains et al., 2012a; Congrains et al., 2012b). LincRNA-p21 enhances p53 activity to regulate the repression of target genes, promoting apoptosis of damaged cells and inhibiting vascular smooth muscle cell proliferation in response to ischemic injury (Huarte et al., 2010; Wu et al., 2014). LIPCAR acts as a biomarker for cardiac remodeling and heart failure post-MI by regulating mitochondrial function and apoptosis, influencing mitochondrial energy production and apoptotic pathways (Kumarswamy et al., 2014). APF promotes autophagy by targeting miR-188-3p, regulating autophagy-related genes, and improving cardiomyocyte survival during ischemic stress (Wang et al., 2015). CAIF inhibits autophagy by suppressing p53-mediated myocardin transcription, reducing excessive cellular component degradation during the acute phase of MI(28). Other lncRNAs involved in MI pathology: H19 regulates VSMC proliferation and apoptosis by acting as a ceRNA for miR-138 and miR-200a, influencing cell growth and apoptosis in atherosclerosis (Li et al., 2009; Gao et al., 2015). Linc00323-003 and MIR503HG modulate endothelial cell function and angiogenesis by regulating VEGF signaling, contributing to vascular homeostasis and repair (Fiedler et al., 2015). HIF1A-AS1 regulates apoptosis and proliferation of vascular endothelial cells by modulating the HIF1A signaling pathway, crucial for the response to hypoxia and ischemia (Wang et al., 2015). MALAT1 influences endothelial cell function and vessel growth by regulating cell cycle genes and alternative splicing of pre-mRNAs (Tripathi et al., 2013; Michalik et al., 2014). Lnc-Ang362 regulates VSMC proliferation and migration by modulating Ang II receptor expression and downstream signaling pathways, critical for vascular remodeling and hypertension (Leung et al., 2013). LncRNA-SENCR regulates endothelial cell migration and proliferation by modulating genes involved in VSMC differentiation and function (Bell et al., 2014). LncLSTR regulates lipid metabolism and homeostasis by modulating genes involved in lipid biosynthesis and transport, impacting lipid levels and atherosclerosis risk (Li et al., 2015). LncRNA RP5-833A20.1 modulates cholesterol homeostasis and inflammatory responses by acting as a ceRNA for miR-382-5p, influencing cholesterol metabolism and inflammatory signaling pathways (Hu et al., 2015). sONE regulates endothelial nitric oxide synthase (eNOS) expression and activity by acting as an antisense RNA, modulating NO production and vascular tone, critical for endothelial function and cardiovascular health (Robb et al., 2004; Fish et al., 2007). Although lncRNAs are generally unstable in cytoplasm (Kumarswamy et al., 2014) and susceptible to degradation, some display structural variations like folding and circularization, and can serve as biomarkers for myocardial infarction (Ounzain et al., 2015; Cai et al., 2016; Yan et al., 2016; Zhang et al., 2016).

Furthermore, keyword analysis reveals the primary research directions in this field, encompassing areas such as lncRNAs expression (Wang et al., 2016), cardiac ischemia/reperfusion injury (Liu et al., 2014; Liu et al., 2015), cell proliferation, and atherosclerosis. Through emerging keyword citation analysis, it is evident that hot topics in this area have evolved over different periods. From early gene association studies (Zangrando et al., 2014; Ounzain et al., 2015) to recent investigations into heart failure (Li et al., 2013; Yang et al., 2014; Di Salvo et al., 2015) and autophagy mechanisms (Wu et al., 2014; Zhang et al., 2019), the field of MI-related lncRNAs has been continually evolving. Autophagy is a critical cytoprotective mechanism during myocardial infarction. Studies have shown that certain lncRNAs, such as APF (Autophagy Promoting Factor) and CAIF (Cardiac Autophagy Inhibitory Factor), play significant roles in regulating autophagy-related gene expression, thereby influencing cardiomyocyte survival and apoptosis. APF promotes autophagy by targeting miR-188-3p (Wang et al., 2015), while CAIF inhibits autophagy by suppressing p53-mediated myocardin transcription (Liu et al., 2018). These findings provide potential targets for developing new therapeutic strategies for myocardial infarction. These research trends may reflect the developmental trajectory and focal points of future studies in this domain. In the context of myocardial infarction and LncRNAs, the frequent appearance of the terms “expression,” “atherosclerosis,” and “apoptosis” highlights their interconnected roles in cardiovascular pathology. “Expression,” lncRNAs regulate gene expression through various mechanisms, including chromatin remodeling, transcriptional regulation, RNA processing, and post-transcriptional regulation. Specifically, MIAT has been identified as a myocardial infarction susceptibility locus in a large-scale case-control study, and is also implicated in diabetic retinopathy, microvascular dysfunction, and neuronal development (Ishii et al., 2006). Additionally, ANRIL interacts with multiple proteins, such as those in the Polycomb complex, to regulate gene expression and influence vascular smooth muscle cell proliferation and atherosclerosis progression (Holdt et al., 2016). Atherosclerosis is a major cause of myocardial infarction, and lncRNAs play a significant role in its development. For example, ANRIL regulates vascular smooth muscle cell proliferation, adhesion, and apoptosis, increasing the risk of coronary artery disease and arterial disease (Holdt et al., 2010). lncRNA H19 is associated with atherosclerosis risk, with polymorphisms in H19 linked to this condition in a Chinese population (Gao et al., 2015). “Apoptosis,” or programmed cell death, lncRNAs are crucial in regulating apoptosis in cardiomyocytes, which is essential for cell survival post-myocardial infarction. For instance, lncRNA ZFAS1 induces mitochondrial-mediated apoptosis by causing cytosolic Ca2⁺ overload (Jiao et al., 2019). Understanding these relationships underscores the significance of LncRNAs in myocardial infarction, offering insights into their potential as focal points for novel therapeutic strategies.

The COVID-19 pandemic has significantly impacted cardiovascular health globally, with evidence suggesting that SARS-CoV-2 infection can lead to myocardial injury and inflammatory responses (Bangalore et al., 2020; Clerkin et al., 2020; Guo et al., 2020; Shi et al., 2020; Zhou et al., 2020). Emerging research indicates that long non-coding RNAs (lncRNAs) may play a crucial role in these processes. For instance, COVID-19 infection has been shown to differentially regulate several lncRNAs, affecting their normal functions and potentially exacerbating cardiovascular complications. The infection induces a robust inflammatory response, often leading to a cytokine storm, which can impact the expression and function of these lncRNAs. For example, MALAT1 is downregulated, possibly diminishing its protective roles. NEAT1 is upregulated, potentially exacerbating inflammation and myocardial damage. These alterations in lncRNA expression and function highlight the complex interplay between viral infection and host cellular mechanisms, underscoring the importance of understanding these interactions for better management of cardiovascular complications in COVID-19 patients (Greco et al., 2020). Moving forward, it is expected that research in this area will focus on understanding the mechanisms by which lncRNAs influence myocardial inflammation and repair in the context of COVID-19, as well as the long-term cardiovascular effects of the virus.

Lifestyle factors such as physical activity, nutrition, and sleep have been shown to significantly affect cardiovascular health and the incidence of MI. Studies have demonstrated that regular physical activity can improve cardiovascular outcomes and reduce the risk of MI (You et al., 2024a). Nutrition, particularly diets rich in fruits, vegetables, and omega-3 fatty acids, has been linked to reduced inflammation and improved cardiovascular health (You et al., 2024b). Additionally, adequate sleep is crucial for maintaining cardiovascular health, with sleep disturbances being associated with an increased risk of MI (You et al., 2024c). While the direct mechanisms linking lifestyle factors to lncRNA expression in the context of MI remain unclear, it is plausible that these factors could influence lncRNA-mediated pathways indirectly through their overall impact on cardiovascular health. Future research should explore these potential interactions to provide a more comprehensive understanding of how lifestyle modifications can be leveraged to prevent and manage MI through lncRNA regulation.

Limitations of this study include its reliance on the WoSCC database (Donthu et al., 2021), which, while comprehensive, may not include all relevant studies. The majority of publications being in English could also introduce selection bias. This study limits its literature review to the period from 2000 to 2023, potentially omitting valuable insights from earlier foundational research.

In summary, significant progress has been made in the field of MI-related lncRNAs over the past few years; however, numerous enigmas and challenges still remain. The sustained growth and international collaboration in this research area will aid in deepening our understanding of the role of lncRNAs in myocardial infarction, and offer more possibilities for the development of new diagnostic methods and therapeutic strategies.

This study serves as a comprehensive guide for emerging scholars in the domain of MI-related lncRNA research. It delineates the evolution of the field, encapsulating historical developments, the current research landscape, and prospective avenues of investigation. By synthesizing these elements, the research furnishes scholars with a robust framework to navigate the intricacies of the field, enabling them to formulate pertinent research inquiries and contribute effectively to the scholarly discourse.

Over the past two decades, the field of MI-related lncRNAs has experienced significant growth, showing an exponential trend. China holds considerable influence in this domain, with collaborations spanning across Asia, North America, and Europe. The research is concentrated in areas including cardiovascular systems, cell biology, and physiology. Our bibliometric analysis reveals critical biological insights into the roles of lncRNAs in MI, particularly their regulatory functions in gene expression, atherosclerosis, and apoptosis. These lncRNAs not only serve as potential biomarkers but also offer promising therapeutic targets for MI. Future studies may likely focus on areas such as circulating microRNAs, heart failure, receptors, targets, and autophagy, which hold high research potential. This bibliometric analysis on MI-related lncRNAs offers a comprehensive perspective on the current status and future trends in this field, providing a framework for integrating bibliometric tools with biological research to advance our understanding and treatment of MI.