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Physical Exercise: A Novel Tool to Protect Mitochondrial Health
Open accessAbstract
Mitochondrial dysfunction is a crucial contributor to heart diseases. Alterations in energetic metabolism affect crucial homeostatic processes, such asATP production, the generation of reactive oxygen species, and the release of pro-apoptotic factors, associated with metabolic abnormalities. In response to energetic deficiency, the cardiomyocytes activate the Mitochondrial Quality Control (MQC), a critical process in maintaining mitochondrial health. This process is compromised in cardiovascular diseases depending on the pathology’s severity and represents, therefore, a potential therapeutic target. Several potential targeting molecules within this process have been identified in the last years, and therapeutic strategies have been proposed to ameliorate mitochondria monitoring and function. In this context, physical exercise is considered a non-pharmacological strategy to protect mitochondrial health. Physical exercise regulates MQC allowing the repair/elimination of damaged mitochondria and synthesizing new ones, thus recovering the metabolic state. In this review, we will deal with the effect of physical exercise on cardiac mitochondrial function tracing its ability to modulate specific steps in MQC both in physiologic and pathologic conditions.
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“Engaging in regular physical activity or exercise training, which proves beneficial for enhancing mitochondrial homeostasis in individuals with sarcopenia, significantly regulates mitophagy, mitochondrial biogenesis, mitochondrial dynamics, and mitochondrial redox biology [9,10,11].”
From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [10]
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Mitochondria: It is all about energy
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Role of Impaired Mitochondrial Dynamics Processes in the Pathogenesis of Alzheimer’s Disease
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Positive Aspects of Oxidative Stress at Different Levels of the Human Body: A Review
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Age-associated inflammation and implications for skeletal muscle responses to exercise
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Metadata
- Authors
- Sorriento, D., Di Vaia, E., & Iaccarino, G.
- Affiliations
- Federico II University Hospital (IT)
- Corresponding author
- Iaccarino, Guido
- Venue
- Frontiers in Physiology
- Publisher
- Frontiers Media SA
- Published
- 2021-04-27
- Volume
- 12
- Pages
- 660068-660068
- ISSN
- 1664-042X (ISSN-L)
- PMC
- PMC8110831
- OpenAlex
- W3158316719
- Cited by
- 118
- References
- 168
- Citations by year
- 2026: 14 · 2025: 35 · 2024: 24 · 2023: 27 · 2022: 15 · 2021: 3
- FWCI
- 1.81
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Physiology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Keywords
- physical activity, mitochondrial quality control, mitochondrial dysfunction, cardiomyocytes, heart disease, reactive oxygen species, apoptosis, ATP production, energy metabolism, non-pharmacological treatment, mitochondrial biogenesis
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