粒体自噬
自噬
线粒体
细胞生物学
缺血
再灌注损伤
人口
生物
医学
内科学
生物化学
细胞凋亡
环境卫生
作者
Yuzhen Li,Xudong Wu,Xiu‐hua Liu,Pei‐feng Li
摘要
Abstract 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.
科研通智能强力驱动
Strongly Powered by AbleSci AI