粒体自噬
医学
心肌病
线粒体生物发生
线粒体
发病机制
神经科学
心脏病学
生物信息学
生物
自噬
心力衰竭
病理
细胞生物学
遗传学
细胞凋亡
作者
Xing Chang,Sam Toan,Ruibin Li,Hao Zhou
出处
期刊:EBioMedicine
[Elsevier]
日期:2022-09-19
卷期号:84: 104260-104260
被引量:64
标识
DOI:10.1016/j.ebiom.2022.104260
摘要
Despite considerable efforts to prevent and treat ischemic cardiomyopathy (ICM), effective therapies remain lacking, in part owing to the complexity of the underlying molecular mechanisms, which are not completely understood yet. It is now widely thought that mitochondria serve as "sentinel" organelles that are capable of detecting cellular injury and integrating multiple stress signals. These pathophysiological activities are temporally and spatially governed by the mitochondrial quality surveillance (MQS) system, involving mitochondrial dynamics, mitophagy, and biogenesis. Dysregulation of MQS is an early and critical process contributing to mitochondrial bioenergetic dysfunction and sublethal injury to cardiomyocytes during ICM. An improved understanding of the pathogenesis of ICM may enable the development of novel preventive and therapeutic strategies aimed at overcoming the challenge of myocardial ischemia and its cardiovascular sequelae. This review describes recent research on the protective effects of MQS in ICM and highlights promising therapeutic targets.
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