Mitophagy in Cardiomyocytes and in Platelets: A Major Mechanism of Cardioprotection Against Ischemia/Reperfusion Injury

被引:47
|
作者
Zhang, Weilin [1 ]
Chen, Chuyan [2 ,3 ]
Wang, Jun [1 ]
Liu, Lei [1 ]
He, Yubin [4 ]
Chen, Quan [1 ]
机构
[1] Chinese Acad Sci, Inst Zool, State Key Lab Membrane Biol, Beijing, Peoples R China
[2] Chinese Acad Med Sci, Beijing, Peoples R China
[3] Peking Union Med Coll, Sch Basic Med, Beijing, Peoples R China
[4] Chinese Army Gen Hosp, Heart Ctr, Dept Cardiol, Beijing, Peoples R China
基金
北京市自然科学基金;
关键词
ISCHEMIA-REPERFUSION INJURY; PERMEABILITY TRANSITION PORE; CYTOCHROME-C-OXIDASE; P2Y(12) RECEPTOR ANTAGONIST; REACTIVE OXYGEN; MYOCARDIAL REPERFUSION; OXIDATIVE STRESS; MITOCHONDRIAL DYSFUNCTION; NLRP3; INFLAMMASOME; RESPIRATORY SUPERCOMPLEX;
D O I
10.1152/physiol.00030.2017
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Mitophagy, a process that selectively removes damaged organelles by autolysosomal degradation, is an early cellular response to ischemia. Mitophagy is activated in both cardiomyocytes and platelets during ischemia/reperfusion (I/R) and heart disease conditions. We focus on the molecular regulation of mitophagy and highlight the role of mitophagy in cardioprotection.
引用
收藏
页码:86 / 98
页数:13
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