Skeletal muscle aging and the mitochondrion
Open accessAbstract
Decline in human muscle mass and strength (sarcopenia) is a hallmark of the aging process. A growing body of research in the areas of bioenergetics and protein turnover has placed the mitochondria at the center of this process. It is now clear that, unless an active lifestyle is rigorously followed, skeletal muscle mitochondrial decline occurs as humans age. Increasing research on mitochondrial biology has elucidated the regulatory pathways involved in mitochondrial biogenesis, many of which are potential therapeutic targets, and highlight the beneficial effects of vigorous physical activity on skeletal muscle health for an aging population.
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In skeletal muscle, reduced mitochondrial respiration has been linked to aberrant control of mitochondrial dynamics.
“In skeletal muscle, reduced mitochondrial respiration has also been linked to aberrant control of mitochondrial dynamics [64–67].”
From Proinflammatory NFkB signalling promotes mitochondrial dysfunction in skeletal muscle in response to cellular fuel overloading (2019) · cites this paper as [64]
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- Authors
- Johnson, M. L., Robinson, M. M., & Nair, K. S.
- Affiliations
- Mayo Clinic (US)
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2013-05
- Volume
- 24
- Issue
- 5
- Pages
- 247-256
- ISSN
- 1043-2760 (ISSN-L)
- PMC
- PMC3641176
- OpenAlex
- W2010512235
- Cited by
- 233
- References
- 104
- Citations by year
- 2026: 17 · 2025: 14 · 2024: 14 · 2023: 16 · 2022: 17 · 2021: 12 · 2020: 26 · 2019: 21 · 2018: 20 · 2017: 15 · 2016: 18 · 2015: 20 · 2014: 15 · 2013: 7 · 2012: 1
- FWCI
- 1.88
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR000135)
- National Institute on Aging (AG-09531, R01AG009531)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK41973, R01DK041973, T32DK007352, T32DK007198)
- National Center for Research Resources (UL1RR024150)
- National Center for Advancing Translational Sciences
- 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 › Adipose Tissue and Metabolism
- Keywords
- skeletal muscle aging, sarcopenia, mitochondria, mitochondrial biogenesis, bioenergetics, protein turnover, physical activity, therapeutic target
- MeSH terms
- Aging, Animals, Humans, Mitochondria, Muscle, Models, Biological, Muscle Proteins, Signal Transduction, Oxidative Stress, Muscle, Skeletal, Mitochondrial Proteins, Mitochondrial Diseases, Protein Stability, Sarcopenia, Mitochondrial Dynamics
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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