Mitophagy imbalance in cardiomyocyte ischaemia/reperfusion injury

被引：28

作者：

Li, Yu-zhen ^{[1
]}

Wu, Xu-dong ^{[2
]}

Liu, Xiu-hua ^{[1
]}

Li, Pei-feng ^{[3
]}

机构：

[1] Peoples Liberat Army Gen Hosp, Inst Basic Med Sci, Dept Pathophysiol, Beijing, Peoples R China

[2] Peoples Liberat Army Gen Hosp, Dept Out Patient, Beijing, Peoples R China

[3] Qingdao Univ, Inst Translat Med, Qingdao, Peoples R China

来源：

ACTA PHYSIOLOGICA | 2019年 / 225卷 / 04期

基金：

中国国家自然科学基金;

关键词：

cardiomyocyte; ischaemia/reperfusion; mitochondria; mitophagy; CARDIAC ISCHEMIA/REPERFUSION INJURY; GROUP BOX 1; MITOCHONDRIAL AUTOPHAGY; NLRP3; INFLAMMASOME; PARKIN; RECEPTOR; UBIQUITIN; FUNDC1; PINK1; HEART;

D O I：

10.1111/apha.13228

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

The rhythmic contraction of cardiomyocytes consumes a lot of energy. 90% of ATP in cardiomyocytes is produced by mitochondria. Maintenance of a healthy population of mitochondria by mitophagy is critical for cardiomyocyte survival and normal function. Mitophagy refers to selective removal of damaged mitochondria by autophagy mechanism. The process of mitophagy must be restricted to dysfunctional mitochondria and maintained at a balanced level. Disruption in the balance inevitably leads to cardiomyocyte injury and dysfunction. Accumulating evidence suggests that mitophagy plays a pivotal role in ischaemia/reperfusion-induced cardiomyocyte injury. In this review, we focus on the current understanding of mitophgy in cardiomyocyte function, the implications for cardiomyocyte injury in response to ischaemia/reperfusion as well as their underlying potential mechanisms.

引用

页数：16

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