Abstract

Cardiovascular disease (CVD) is the leading cause of death in the global population, accounting for about one-third of all deaths each year. Notably, with CVDs, myocardial damages result from myocardial infarction (MI) or cardiac arrhythmias caused by interrupted blood flow. Significantly, in the process of MI or myocardial ischemic-reperfusion (I/R) injury, both regulated and non-regulated cell death methods are involved. The critical factor for patients’ prognosis is the infarct area’s size, which determines the myocardial cells’ survival. Cell therapy for MI has been a research hotspot in recent years; however, exosomes secreted by cells have attracted much attention following shortcomings concerning immunogens. Exosomes are extracellular vesicles containing several biologically active substances such as lipids, nucleic acids, and proteins. New evidence suggests that exosomes play a crucial role in regulating cell death after MI as exosomes of various stem cells can participate in the cell damage process after MI. Hence, in the review herein, we focused on introducing various cell-derived exosomes to reduce cell death after MI by regulating the cell death pathway to understand myocardial repair mechanisms better and provide a reference for clinical treatment.

Highlights

  • Despite the considerable improvements in healthcare worldwide, acute myocardial infarction (MI) has long been the primary cause of death from coronary heart diseases (Roth et al, 2017)

  • We discussed the anti-cell death potential of various exosomes from different cells, primarily stem cells for heart injury caused by MI or I/R

  • Studies have found that after LPS pretreated stem cells, their exosomes can enhance the M1 polarization of macrophages (Kang et al, 2018). All these indicate that modified and/or unmodified stem cells can increase the production of protective substances when they perceive danger signals, and exosomes serve as media to deliver protective substances

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Summary

Introduction

Despite the considerable improvements in healthcare worldwide, acute myocardial infarction (MI) has long been the primary cause of death from coronary heart diseases (Roth et al, 2017). Studies have shown that the basic autophagy process in cardiomyocytes is upregulated via the AMPK-mTOR signaling pathway, leading to reduced MI in animal models of acute MI (Foglio et al, 2017). On the contrary, during reperfusion, ALDH2 can inhibit autophagy by activating Akt and mTOR, thereby protecting cardiomyocytes from cell death caused by hypoxia and reoxygenation (Ma et al, 2011).

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