线粒体
粒体自噬
医学
再灌注损伤
药理学
缺血
线粒体分裂
线粒体DNA
线粒体通透性转换孔
线粒体ROS
生物
心脏病学
细胞生物学
生物化学
细胞凋亡
程序性细胞死亡
自噬
基因
作者
Jinfu Peng,Oluwabukunmi Modupe Salami,Lei Cai,Dan Ni,Olive Habimana,Guanghui Yi
标识
DOI:10.1080/1061186x.2022.2085728
摘要
Myocardial ischaemia-reperfusion injury (MI/RI) refers to the further damage done to ischaemic cardiomyocytes when restoring blood flow. A large body of evidence shows that MI/RI is closely associated with excessive production of mitochondrial reactive oxygen species, mitochondrial calcium overload, disordered mitochondrial energy metabolism, mitophagy, mitochondrial fission, and mitochondrial fusion. According to the way it affects mitochondria, it can be divided into mitochondrial quality abnormalities and mitochondrial quantity abnormalities. Abnormal mitochondrial quality refers to the dysfunction caused by the severe destruction of mitochondria, which then affects the balance of mitochondrial density and number, causing an abnormal mitochondrial quantity. In the past, most of the reports were limited to the study of the mechanism of myocardial ischaemia-reperfusion injury, some of which involved mitochondria, but no specific countermeasures were proposed. In this review, we outline the mechanisms for treating myocardial ischaemia-reperfusion injury from the direction of mitochondria and focus on targeted interventions and drugs to restore mitochondrial health during abnormal mitochondrial quality control and abnormal mitochondrial quantity control. This is an update in the field of myocardial ischaemia-reperfusion injury.
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