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

被引:51
作者
Wu, Xun [1 ]
Iroegbu, Chukwuemeka Daniel [1 ]
Peng, Jun [2 ]
Guo, Jianjun [3 ]
Yang, Jinfu [1 ]
Fan, Chengming [1 ,2 ,3 ]
机构
[1] Cent South Univ, Xiangya Hosp 2, Dept Cardiovasc Surg, Changsha, Peoples R China
[2] Hunan Prov Key Lab Cardiovasc Res, Changsha, Peoples R China
[3] Hunan Fangsheng Pharmaceut Co Ltd, Changsha, Peoples R China
基金
中国国家自然科学基金;
关键词
myocardial infarction; apoptosis; autophagy-dependent death; pyroptosis; ferroptosis; exosomes; microRNA; myocardial protection; BCL-2 PROTEIN FAMILY; OXIDATIVE STRESS; CARDIOMYOCYTE APOPTOSIS; INFLAMMATORY CASPASES; ENERGY HOMEOSTASIS; NLRP3; INFLAMMASOME; CARDIAC REPAIR; GASDERMIN D; AUTOPHAGY; INJURY;
D O I
10.3389/fcell.2021.673677
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
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.
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页数:13
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