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

Frontiers in Cell and Developmental Biology

Xun Wu¹  Chukwuemeka Daniel Iroegbu¹  Jinfu Yang¹  Jianjun Guo²  Chengming Fan²  Jun Peng³ 

[1] Department of Cardiovascular Surgery, The Second Xiangya Hospital, Central South University, Changsha, China;Hunan Fangsheng Pharmaceutical Co., Ltd., Changsha, China;Hunan Provincial Key Laboratory of Cardiovascular Research, Changsha, China;

关键词: myocardial infarction;    apoptosis;    autophagy-dependent death;    pyroptosis;    ferroptosis;    exosomes;   

DOI  :  10.3389/fcell.2021.673677

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown