Insights into research on myocardial ischemia/reperfusion injury from 2012 to 2021: a bibliometric analysis

Abstract

Background Numerous studies on myocardial ischemia/reperfusion (MI/R) injury have been undertaken in recent years. Hotspots and developmental trends in MI/R research are being rapidly updated. However, there has been no bibliometric analysis that systematically evaluates existing literature on MI/R injury. Our study explores developments in MI/R research over the past decade, and provides a reference for future research. Materials and methods Both experimental and clinical publications on MI/R injury from 2012 to 2021 were retrieved from the Web of Science Core Collection database. The CiteSpace and VOSviewer tools were used to perform a bibliometric analysis. Results A total of 8419 papers were analyzed. The number of annual publications demonstrated an overall upward trend, rising from 629 publications in 2012 to 1024 publications in 2021. China, the USA, Germany, England, and Italy were the top five contributors to MI/R studies. The Fourth Military Medical University in China contributed the most publications (188, 2.23%), while the University College London in England cooperated the most with relevant research institutions. Derek J Hausenloy (University College London), Derek M Yellon (University College London), and Gerd Heusch (University of Essen Medical School) were the top three most active and influential scholars according to the H-index. Among the top 10 journals with the most publications, Basic Research in Cardiology had the highest impact factors. The top three co-cited journals were Circulation, Circulation Research, and Cardiovascular Research. According to a co-cited reference analysis, MI/R research can be divided across 10 major subfields of mitophagy, cardioprotection, inflammation, remote ischemic preconditioning, long non-coding RNA, melatonin, postconditioning, mitochondria, microvascular obstruction, and ferroptosis. After 2018, the keywords with strongest citation bursts included extracellular vesicles, long non-coding RNA, cell proliferation, microRNA, mitochondrial quality control, mitophagy, biomarker, and mitochondrial biogenesis. Conclusions The present study reveals the influential authors, cooperating institutions, and main research foci in the field of MI/R injury in the past decade. The latest hotspots are a more in-depth insight into the molecular mechanisms underlying MI/R injury, such as mitochondrial quality control, non-coding RNAs, cell proliferation, and extracellular vesicles.

Circular RNA HIPK3 facilitates ferroptosis in gestational diabetes mellitus by regulating glutathione peroxidase 4 DNA methylation

“…40 In the present study, we investigated the role of circHIPK3, a functional circRNA, in diverse diseases. 21,41 Placental tissues and plasma specimens, frequently utilized as experimental materials, [42][43][44] were collected from pregnant women to estimate circHIPK3 levels in these samples. The expression of circHIPK3 increased evidently in GDM placental tissues and plasma samples compared to that in GDM-free samples.…”

“…Circ‐PNPT1 facilitates GDM by modulating the miR‐889‐3p/PAK1 axis in trophoblast cells 40 . In the present study, we investigated the role of circHIPK3, a functional circRNA, in diverse diseases 21,41 . Placental tissues and plasma specimens, frequently utilized as experimental materials, 42–44 were collected from pregnant women to estimate circHIPK3 levels in these samples.…”

The potential of circHIPK3 as a biomarker in chronic myeloid leukemia

“…In myocardial ischemia, Bai et al. demonstrated that circHIPK3 inhibits proliferative capacity and induces heart cells to apoptosis by binding with miR-124-3p ( 31 ). Chaofang Lian et al.…”

lncRNA Oip5-as1 inhibits excessive mitochondrial fission in myocardial ischemia/reperfusion injury by modulating DRP1 phosphorylation

“…Previous studies have demonstrated that MI/R injury results from a complex interplay of pathological events upon reperfusion, including oxidative stress, inflammatory responses, and mitochondrial dysfunction [ 4 ]. Despite these insights, developing effective therapeutic agents to target MI/R injury remains challenging [ 2 – 5 ]. This underscores the need for a deeper understanding of its molecular mechanisms and the identification of novel therapeutic targets.…”