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线粒体自噬:分子机制与心血管疾病的关系。

Mitochondrial autophagy: molecular mechanisms and implications for cardiovascular disease.

机构信息

Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.

Department of Pharmacy, Shanghai East Hospital, Tongji University, Shanghai, 200120, China.

出版信息

Cell Death Dis. 2022 May 9;13(5):444. doi: 10.1038/s41419-022-04906-6.

Abstract

Mitochondria are highly dynamic organelles that participate in ATP generation and involve calcium homeostasis, oxidative stress response, and apoptosis. Dysfunctional or damaged mitochondria could cause serious consequences even lead to cell death. Therefore, maintaining the homeostasis of mitochondria is critical for cellular functions. Mitophagy is a process of selectively degrading damaged mitochondria under mitochondrial toxicity conditions, which plays an essential role in mitochondrial quality control. The abnormal mitophagy that aggravates mitochondrial dysfunction is closely related to the pathogenesis of many diseases. As the myocardium is a highly oxidative metabolic tissue, mitochondria play a central role in maintaining optimal performance of the heart. Dysfunctional mitochondria accumulation is involved in the pathophysiology of cardiovascular diseases, such as myocardial infarction, cardiomyopathy and heart failure. This review discusses the most recent progress on mitophagy and its role in cardiovascular disease.

摘要

线粒体是高度动态的细胞器,参与 ATP 生成,并涉及钙稳态、氧化应激反应和细胞凋亡。功能失调或受损的线粒体可能会导致严重后果,甚至导致细胞死亡。因此,维持线粒体的内稳态对于细胞功能至关重要。自噬是线粒体毒性条件下选择性降解受损线粒体的过程,在维持线粒体质量控制方面起着至关重要的作用。加剧线粒体功能障碍的异常自噬与许多疾病的发病机制密切相关。由于心肌是一种高度氧化代谢的组织,线粒体在维持心脏的最佳性能方面起着核心作用。功能失调的线粒体积累参与了心血管疾病的病理生理学,如心肌梗死、心肌病和心力衰竭。本文综述了自噬及其在心血管疾病中的作用的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63ca/9085840/c7ffd71118e5/41419_2022_4906_Fig1_HTML.jpg

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