Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling.

Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling.
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线粒体自噬:压力过载引起的心脏重塑的潜在目标

DOI:
10.1155/2022/2849985
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发表时间:
2022
影响因子:
--
通讯作者:
Chen, Mao
Chen, Mao
中科院分区:
生物学2区
文献类型:
--
作者:
Shao, Ruochen;Li, Junli;Qu, Tianyi;Liao, Yanbiao;Chen, Mao

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压力超负荷引起的心脏重塑和心功能障碍的病理机制尚不清楚。线粒体损伤和功能障碍,包括线粒体生物能紊乱、氧化应激和线粒体DNA损伤,会导致压力超负荷引起的心脏损伤。线粒体自噬是线粒体稳态和功能的重要调节因子,由线粒体损伤引发,参与心血管疾病的病理过程。最近的研究表明,线粒体自噬在压力超负荷模型中起着至关重要的作用,但线粒体自噬异常与压力超负荷引起的心脏损伤之间因果关系的证据尚无定论。本文总结了压力超载模型中线粒体自噬的机制、作用和调节。它还特别关注可能在压力超负荷时调节线粒体自噬的活性化合物,这为可能的临床应用提供了线索。
The pathological mechanisms underlying cardiac remodelling and cardiac dysfunction caused by pressure overload are poorly understood. Mitochondrial damage and functional dysfunction, including mitochondrial bioenergetic disorder, oxidative stress, and mtDNA damage, contribute to heart injury caused by pressure overload. Mitophagy, an important regulator of mitochondrial homeostasis and function, is triggered by mitochondrial damage and participates in the pathological process of cardiovascular diseases. Recent studies indicate that mitophagy plays a critical role in the pressure overload model, but evidence on the causal relationship between mitophagy abnormality and pressure overload-induced heart injury is inconclusive. This review summarises the mechanism, role, and regulation of mitophagy in the pressure overload model. It also pays special attention to active compounds that may regulate mitophagy in pressure overload, which provide clues for possible clinical applications.
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