Mesenchymal stem cell‐derived exosomes in myocardial infarction: Therapeutic potential and application

Abstract

Myocardial infarction refers to the irreversible impairment of cardiac function resulting from the permanent loss of numerous cardiomyocytes and the formation of scar tissue. This condition is caused by acute and persistent inadequate blood supply to the heart's arteries. In the treatment of myocardial infarction, Mesenchymal stem cells (MSCs) play a crucial role because of their powerful therapeutic effects.These effects primarily stem from the paracrine secretion of multiple factors by MSCs, with exosome‐carried microRNAs being the most effective component in promoting cardiac function recovery after infarction. Exosome therapy has emerged as a promising cell‐free treatment for myocardial infarction as a result of its relatively simple composition, low immunogenicity and controlled transplantation dose. Despite these advantages, maintaining the stability of exosomes after transplantation and enhancing their targeting effect remain significant challenges in clinical applications. In recent developments, several approaches have been designed to optimize exosome therapy. These include enhancing exosome retention, improving their ability to target specific effects, pretreating MSC‐derived exosomes and employing transgenic MSC‐derived exosomes. This review primarily focuses on describing the biological characteristics of exosomes, their therapeutic potential and their application in treating myocardial infarction.

Release of exosomes from injectable silk fibroin and alginate composite hydrogel for treatment of myocardial infarction

“…However, it is not possible to completely prevent microvascular dysfunction after treatment, and therapy does not reverse myocardial necrosis or substantially improve cardiac function. 2 Thus, the ideal treatment for myocardial infarction is to promote hemostasis and angiogenesis, leading to a significant reduction in apoptosis and necrosis factors in cardiomyocytes. Traditional treatment methods are inadequate at inducing cell regeneration and, as a result, are unable to effectively address the underlying cause of reduced cardiac function.…”