Mitochondrial Dysfunction in HFpEF: Potential Interventions Through Exercise
- PMID: 39863753
- DOI: 10.1007/s12265-025-10591-5
Mitochondrial Dysfunction in HFpEF: Potential Interventions Through Exercise
Abstract
HFpEF is a prevalent and complex type of heart failure. The concurrent presence of conditions such as obesity, hypertension, hyperglycemia, and hyperlipidemia significantly increase the risk of developing HFpEF. Mitochondria, often referred to as the powerhouses of the cell, are crucial in maintaining cellular functions, including ATP production, intracellular Ca2+ regulation, reactive oxygen species generation and clearance, and the regulation of apoptosis. Exercise plays a vital role in preserving mitochondrial homeostasis, thereby protecting the cardiovascular system from acute stress, and is a fundamental component in maintaining cardiovascular health. In this study, we review the mitochondrial dysfunction underlying the development and progression of HFpEF. Given the pivotal role of exercise in modulating cardiovascular diseases, we particularly focus on exercise as a potential therapeutic strategy for improving mitochondrial function. Graphical abstract Note: This picture was created with BioRender.com.
Keywords: Exercise; Heart failure with preserved ejection fraction; Mitochondria; Mitochondrial dynamics; Oxidative stress.
© 2025. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
Conflict of interest statement
Declarations. Disclosures: Dr. Junjie XIAO is an associate editor of Journal of Cardiovascular Translational Research. Dr. Lijun Wang is an editorial board member of Journal of Cardiovascular Translational Research. The other authors declare no competing interests. Ethics Approval and Consent to Participate: Not applicable. Informed Consent: Not applicable.
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