Key Takeaways & Executive Findings
- •• Mitophagy is a new target for the prevention and treatment of cardiovascular diseases. • Exercise can regulate mitophagy through multiple pathways. • Exercise intervention can exert cardiovascular protective effects by regulating mitophagy. • Different exercise modalities have distinct mechanisms in regulating mitophagy.
Abstract
BACKGROUND: Mitophagy plays a crucial regulatory role in the occurrence and development of cardiovascular diseases. Exercise intervention can mediate mitophagy to improve cardiovascular function, which provides new insights for the clinical prevention and treatment of cardiovascular diseases. OBJECTIVE: To summarize the regulatory role of mitophagy in cardiovascular diseases, the influence of exercise on mitophagy, and the mechanism by which exercise-mediated mitophagy improves cardiovascular diseases. METHODS: PubMed and CNKI databases were searched for relevant literature using the search terms of “mitophagy, mitochondrial function, cardiovascular disease, aerobic exercise, resistance training, combined aerobic resistance exercise, high-intensity interval training” in Chinese and English, respectively. Based on the inclusion and exclusion criteria, totally 88 documents were finally included for summary and analysis. RESULTS AND CONCLUSION: (1) Mitophagy plays a crucial role in the regulation of cardiovascular diseases such as heart failure, myocardial hypertrophy, atherosclerosis, and myocardial ischemia-reperfusion injury. Moreover, mitophagy imbalance or disorder can exacerbate the pathological process of cardiovascular diseases. (2) Various exercise modalities can activate mitophagy by regulating the expression of mitophagy-related factors. Among them, aerobic exercise can promote the formation of autophagosomes, thereby enhancing the regulation of mitophagy; resistance exercise can regulate mitochondrial biogenesis; combined aerobic and resistance exercise can further influence mitophagy by promoting lysosomal biogenesis; high-intensity interval training enhances mitophagy function by regulating the expression of mitochondrial dynamics-related proteins. (3) Exercise regulates mitophagy to alleviate myocardial fibrosis, inhibit cardiomyocyte apoptosis, regulate myocardial oxidative stress, and improve endothelial cell function, thereby playing a key role in the prevention and treatment of cardiovascular diseases, providing a new perspective for exercise promoting health and preventing cardiovascular diseases.
1. Introduction
Cardiovascular diseases are one of the leading causes of death worldwide and have become a major public health challenge threatening human health and life safety [1]. Cardiovascular diseases mainly include heart failure, myocardial hypertrophy, atherosclerosis, and myocardial ischemia-reperfusion injury. Current clinical treatment mainly relies on drug interventions, such as antiplatelet drugs, lipid-lowering drugs, and drugs that improve cardiac function. These drugs have significant advantages in improving the prognosis of patients with cardiovascular diseases and delaying disease progression. However, drug treatment has certain adverse reactions, and the overall morbidity and mortality of cardiovascular diseases remain high globally [2]. Therefore, there is an urgent need to explore safer and more sustainable prevention and treatment strategies.
In recent years, researchers have discovered the key role of mitochondrial dysfunction in the pathogenesis of cardiovascular diseases. As an important regulatory mechanism for maintaining mitochondrial quality control and functional homeostasis, mitophagy has gradually become an important target and potential intervention strategy for the prevention and treatment of cardiovascular diseases. Studies have found that changes in mitophagy-related signaling pathways can affect mitochondrial activity, thereby influencing the occurrence and development of cardiovascular diseases [3]. Recent studies have shown that reasonable exercise intervention can effectively improve myocardial function and vascular endothelial function in patients with cardiovascular diseases.
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JI Long, GONG Guopan, KONG Xiangkui, JIN Pan, CHEN Ziyang, PU Rui (2026). The role of exercise-regulated mitophagy in cardiovascular diseases. Chinese Journal of Tissue Engineering Research. https://doi.org/10.12307/2026.21247
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Frequently Asked Questions
What is mitophagy?
Mitophagy is a selective autophagic process that delivers damaged or dysfunctional mitochondria to lysosomes for degradation, playing a crucial role in maintaining cellular homeostasis and metabolic balance.
How does exercise regulate mitophagy in cardiovascular diseases?
Exercise activates mitophagy-related signaling pathways such as PINK1/Parkin, BNIP3/NIX, and FUNDC1, thereby regulating mitochondrial function and quality control, which exerts beneficial effects in the prevention and treatment of cardiovascular diseases.
What are the different effects of various exercise modalities on mitophagy?
Aerobic exercise promotes autophagosome formation, resistance exercise regulates mitochondrial biogenesis, combined aerobic and resistance exercise promotes lysosomal biogenesis, and high-intensity interval training enhances mitophagy by regulating mitochondrial dynamics-related proteins.
What is the role of mitophagy in cardiovascular diseases?
Mitophagy plays a crucial role in the regulation of heart failure, myocardial hypertrophy, atherosclerosis, and myocardial ischemia-reperfusion injury. Dysregulation of mitophagy can exacerbate the pathological progression of these diseases.
What are the potential mechanisms by which exercise improves cardiovascular diseases through mitophagy?
Exercise regulates mitophagy to alleviate myocardial fibrosis, inhibit cardiomyocyte apoptosis, regulate myocardial oxidative stress, and improve endothelial cell function, thereby contributing to the prevention and treatment of cardiovascular diseases.
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