Key result
Extracellular vesicles play a dual role in AMI by both exacerbating injury and facilitating repair.
Why the study?
Extracellular vesicles play significant dual regulatory roles in acute myocardial infarction pathophysiology, requiring a comprehensive synthesis to establish a foundation for their clinical translation in cardiovascular disease.
Extracellular vesicles play a complex, dual role in acute myocardial infarction pathophysiology, presenting novel opportunities for diagnostic biomarkers and targeted cardiovascular therapies.
May guide EV biomarker development in AMI; leaves open therapeutic validation in prospective trials.
Extracellular vesicles (EVs) are nanoscale particles secreted by cells, encapsulating a variety of biomolecules, and have emerged as significant players in the pathophysiology of acute myocardial infarction (AMI). These vesicles exhibit both detrimental and therapeutic effects. On one hand, EVs contribute to AMI progression by promoting apoptosis, exacerbating inflammatory responses, and impairing angiogenesis. On the other hand, they facilitate cardiac repair by enhancing neovascularization, mitigating programmed cell death, and inhibiting fibrosis. This review provides a comprehensive overview of EV biogenesis, release mechanisms, and their dual regulatory roles in AMI, emphasizing the complex interplay of EVs in myocardial injury. Additionally, it explores the potential of EVs as diagnostic biomarkers and therapeutic delivery vehicles, highlighting their importance in advancing diagnostic and therapeutic strategies. By elucidating the multifaceted roles of EVs, this review aims to establish a foundation for their clinical translation, improve their applicability in precision medicine, and explore the promising potential in cardiovascular disease treatment.
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Wu et al. (2025) conducted a review in Acute myocardial infarction. Extracellular vesicles was evaluated. Extracellular vesicles play a dual role in acute myocardial infarction by both exacerbating injury through apoptosis and inflammation, and facilitating cardiac repair via angiogenesis and reduced fibrosis.
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