Extracellular Vesicles as Emerging Regulators in Ischemic and Hypertrophic Cardiovascular Diseases: A Review of Pathogenesis and Therapeutics
Min Chen, Yanming Wu, Cheng Chen
Abstract
Extracellular vesicles (EVs), including exosomes, microvesicles, and apoptotic bodies, have emerged as important regulators in specific cardiovascular conditions such as myocardial infarction, atherosclerosis, coronary artery disease, and cardiac hypertrophy. EVs mediate intercellular communication by transferring bioactive cargo such as proteins, lipids, and nucleic acids. EVs influence crucial pathological processes, including inflammation, fibrosis, apoptosis, and cardiac remodeling, contributing to disease progression. This review assessed the therapeutic potential of stem cell-derived EVs in reducing inflammation, enhancing angiogenesis, modulating immune responses, and mitigating cardiac remodeling. Specific EV-derived miRNAs such as miR-146a, miR-181b, and miR-21 exhibited beneficial effects in promoting cardiac repair, reducing fibrosis, and improving cardiac function after injury. Special focus is placed on stem cell-derived EVs, which show promise in reducing myocardial injury, promoting angiogenesis, and attenuating pathological hypertrophy. Moreover, we explore the emerging concept of EVs as biomarkers, with circulating endothelial- and platelet-derived EVs correlating with vascular dysfunction, plaque instability, and pro-coagulant activity in clinical studies. Despite their therapeutic promise, the clinical translation of EV-based strategies faces challenges, including lack of standardized isolation protocols, heterogeneity of EV subpopulations, and limited in vivo targeting specificity. Addressing these barriers will be essential to harness EVs as next-generation diagnostic tools and cell-free therapeutic agents. This article reviews the emerging roles of extracellular vesicles, including exosomes, microvesicles, and apoptotic bodies, in atherosclerosis, myocardial ischemia, infarction and reperfusion injury, and cardiac hypertrophy.