Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy
Open accessAbstract
Muscle loss during aging and disuse is a highly prevalent and disabling condition, but knowledge about cellular pathways mediating muscle atrophy is still limited. Given the postmitotic nature of skeletal myocytes, the maintenance of cellular homeostasis relies on the efficiency of cellular quality control mechanisms. In this scenario, alterations in mitochondrial function are considered a major factor underlying sarcopenia and muscle atrophy. Damaged mitochondria are not only less bioenergetically efficient, but also generate increased amounts of reactive oxygen species, interfere with cellular quality control mechanisms, and display a greater propensity to trigger apoptosis. Thus, mitochondria stand at the crossroad of signaling pathways that regulate skeletal myocyte function and viability. Studies on these pathways have sometimes provided unexpected and counterintuitive results, which suggests that they are organized into a complex, heterarchical network that is currently insufficiently understood. Untangling the complexity of such a network will likely provide clinicians with novel and highly effective therapeutics to counter the muscle loss associated with aging and disuse. In this review, we summarize the current knowledge on the mechanisms whereby mitochondrial dysfunction intervenes in the pathogenesis of sarcopenia and disuse atrophy, and highlight the prospect of targeting specific processes to treat these conditions.
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Loss of mitochondrial function with aging is shared by muscle cells and motor neurons.
“It is interesting that a loss of mitochondria function with aging is a mechanism that is shared by both muscle cells (18, 63) and motor neurons (123).”
From Mitochondria initiate and regulate sarcopenia (2017) · cites this paper as [18]
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- Authors
- Calvani, R., Joseph, A.-M., Adhihetty, P. J., Miccheli, A., Bossola, M., Leeuwenburgh, C., Bernabei, R., & Marzetti, E.
- Affiliations
- National Research Council (IT)
- University of Florida (US)
- Sapienza University of Rome (IT)
- Università Cattolica del Sacro Cuore (IT)
- Corresponding author
- Marzetti, Emanuele
- ORCID
- Venue
- bchm
- Publisher
- Walter de Gruyter GmbH
- Published
- 2013-02-02
- Volume
- 394
- Issue
- 3
- Pages
- 393-414
- ISSN
- 1431-6730 (ISSN-L)
- 1437-4315
- PMC
- PMC3976204
- OpenAlex
- W2091503455
- Cited by
- 328
- References
- 186
- Citations by year
- 2026: 16 · 2025: 23 · 2024: 21 · 2023: 22 · 2022: 25 · 2021: 27 · 2020: 43 · 2019: 27 · 2018: 29 · 2017: 29 · 2016: 14 · 2015: 20 · 2014: 22 · 2013: 10
- FWCI
- 1.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biological Chemistry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Funders
- University of Florida (1 P30 AG028740)
- National Institute on Aging (AG-21042, R01AG021042, R01-AG21042, P30AG028740)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK090115, RO1-DK090115-01A1, R01-DK090115-01A1, DK090115)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Keywords
- sarcopenia, disuse atrophy, mitochondrial dysfunction, skeletal muscle, aging, reactive oxygen species, apoptosis, cell quality control, mitochondrial pathway
- MeSH terms
- Humans, Mitochondria, Signal Transduction, Oxidative Stress, Muscular Disorders, Atrophic, Sarcopenia
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