Advances in Cardiotoxicity Induced by Altered Mitochondrial Dynamics and Mitophagy

Mitochondria are the most abundant organelles in cardiac cells, and are essential to maintain the normal cardiac function, which requires mitochondrial dynamics and mitophagy to ensure the stability of mitochondrial quantity and quality. When mitochondria are affected by continuous injury factors, t...

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Bibliographic Details
Published inFrontiers in cardiovascular medicine Vol. 8; p. 739095
Main Authors Yin, Yiyuan, Shen, Haitao
Format Journal Article
LanguageEnglish
Published Frontiers Media S.A 20.09.2021
Subjects
cardiotoxicity
Cardiovascular Medicine
mitochondrial dynamics
mitochondrial fission
mitochondrial fusion
mitophagy
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Summary:Mitochondria are the most abundant organelles in cardiac cells, and are essential to maintain the normal cardiac function, which requires mitochondrial dynamics and mitophagy to ensure the stability of mitochondrial quantity and quality. When mitochondria are affected by continuous injury factors, the balance between mitochondrial dynamics and mitophagy is broken. Aging and damaged mitochondria cannot be completely removed in cardiac cells, resulting in energy supply disorder and accumulation of toxic substances in cardiac cells, resulting in cardiac damage and cardiotoxicity. This paper summarizes the specific underlying mechanisms by which various adverse factors interfere with mitochondrial dynamics and mitophagy to produce cardiotoxicity and emphasizes the crucial role of oxidative stress in mitophagy. This review aims to provide fresh ideas for the prevention and treatment of cardiotoxicity induced by altered mitochondrial dynamics and mitophagy.
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Reviewed by: Pritesh Jain, University of California, San Diego, United States; Stephen C. Kolwicz Jr, Ursinus College, United States
Edited by: Haiyang Tang, University of Arizona, United States
This article was submitted to Cardiovascular Metabolism, a section of the journal Frontiers in Cardiovascular Medicine
ISSN:2297-055X
2297-055X
DOI:10.3389/fcvm.2021.739095