Abstract
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.
Highlights
As the body’s “power plant,” heart is the body’s largest oxygen and energy consumption organ
Hypoxia can activate poly (ADP-ribose) polymerase (PARP), promoting mitophagy by regulating mitochondrial membrane potential and inducing cardiomyocyte apoptosis, reactive oxygen species (ROS) is central for PARP mediated mitochondrial membrane potential ( Ψ m) decline, and inhibited PARP can reduce the production after injury [80]
Shaftaside and MYLS22 can effectively inhibit the expression of dynamin-related protein 1 (DRP1) and optic atrophy protein 1 (OPA1) to inhibit mitochondrial fission and reduce the cardiotoxicity induced by hypoxia, oxidative stress, hyperglycemia and poisoning [231]
Summary
Specialty section: This article was submitted to Cardiovascular Metabolism, a section of the journal Frontiers in Cardiovascular Medicine. 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. 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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