粒体自噬
缺血
医学
线粒体生物发生
再灌注损伤
心肌梗塞
线粒体
蛋白质稳态
心脏病学
内科学
细胞凋亡
生物
细胞生物学
自噬
生物化学
作者
Jin Wang,Sam Toan,Hao Zhou
标识
DOI:10.1016/j.phrs.2020.104771
摘要
Thrombolytic therapy and revascularization strategies create a complete recanalization of the occluded epicardial coronary artery in patients with myocardial infarction (MI). However, about 35 % of patients still experience an impaired myocardial reperfusion, which is termed a no-reflow phenomenon mainly caused by cardiac microvascular ischemia-reperfusion (I/R) injury. Mitochondria are essential for microvascular endothelial cells' survival, both because of their roles as metabolic energy producers and as regulators of programmed cell death. Mitochondrial structure and function are regulated by a mitochondrial quality control (MQC) system, a series of processes including mitochondrial biogenesis, mitochondrial dynamics/mitophagy, mitochondrial proteostasis, and mitochondria-mediated cell death. Our review discusses the MQC mechanisms and how they are linked to cardiac microvascular I/R injury. Additionally, we will summarize the molecular basis that results in defective MQC mechanisms and present potential therapeutic interventions for improving MQC in cardiac microvascular I/R injury.
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