Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion

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.

Beclin1 controls caspase-4 inflammsome activation and pyroptosis in mouse myocardial reperfusion-induced microvascular injury

“…Several forms of cells death have been described, including apoptosis, necroptosis and pyroptosis, and they display different cellular and molecular processes and distinct outcomes. Recently, roles for pyroptosis in cardiovascular disease are emerging, including myocardial infarction, ischemia–reperfusion, diabetic cardiomyopathy and atherosclerosis [ 7 – 9 ]. Pyroptosis, an inflammatory programmed cell death mediated by gasdermin D (GSDMD), is triggered by cytosolic sensing of invasive infection and danger signals.…”

An Emerging Frontier in Intercellular Communication: Extracellular Vesicles in Regeneration

“…Additional reports of EVs that promote cell survival in both in vivo and in vitro injury models exist, although the precise mechanisms by which these EVs act are not as well understood ( Wu et al, 2021 ). EVs also promote apoptosis, for example by transporting Caspase-1 and Gasdermin D from monocytes to pulmonary vascular endothelial cells in an in vitro model of acute lung injury ( Mitra et al, 2018 ).…”

Non-coding RNAs to regulate cardiomyocyte proliferation: A new trend in therapeutic cardiac regeneration

“…During the MI process or myocardial ischemia-reperfusion (I/R) injury, both regulated and non-regulated cell death processes are involved. Later, scar tissue formation will follow this initial injury response ( 24 ). Hence, understanding the heart's regenerative capacity is the primary goal of cardiac regenerative medicine.…”