Myocardial injury: where inflammation and autophagy meet

被引:14
|
作者
Liu, Chunping [1 ,2 ,3 ]
Liu, Yanjiao [2 ]
Chen, Huiqi [2 ]
Yang, Xiaofei [2 ]
Lu, Chuanjian [2 ,3 ]
Wang, Lei [2 ]
Lu, Jiahong [1 ]
机构
[1] Univ Macau, Inst Chinese Med Sci, State Key Lab Qual Res Chinese Med, Taipa, Macau, Peoples R China
[2] Guangzhou Univ Chinese Med, Affiliated Hosp 2, State Key Lab Dampness Syndrome Chinese Med, Guangzhou 51080, Peoples R China
[3] Guangdong Hong Kong Macau Joint Lab Chinese Med &, Guangzhou 510080, Peoples R China
基金
中国国家自然科学基金;
关键词
Autophagy; Inflammation; Myocardial injury; REGULATORY T-CELLS; DIABETIC CARDIOMYOPATHY; REPERFUSION INJURY; PROTECTS HEART; INFARCTION; OVEREXPRESSION; ENHANCEMENT; MACROPHAGES; MECHANISMS; INDUCTION;
D O I
10.1093/burnst/tkac062
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Autophagy is a highly conserved bulk degradation mechanism that degrades damaged organelles, aged proteins and intracellular contents to maintain the homeostasis of the intracellular microenvironment. Activation of autophagy can be observed during myocardial injury, during which inflammatory responses are strongly triggered. Autophagy can inhibit the inflammatory response and regulate the inflammatory microenvironment by removing invading pathogens and damaged mitochondria. In addition, autophagy may enhance the clearance of apoptotic and necrotic cells to promote the repair of damaged tissue. In this paper, we briefly review the role of autophagy in different cell types in the inflammatory microenvironment of myocardial injury and discuss the molecular mechanism of autophagy in regulating the inflammatory response in a series of myocardial injury conditions, including myocardial ischemia, ischemia/reperfusion injury and sepsis cardiomyopathy.
引用
收藏
页数:15
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