Genetically enhancing mitochondrial antioxidant activity improves muscle function in aging
Open accessAbstract
Age-related skeletal muscle dysfunction is a leading cause of morbidity that affects up to half the population aged 80 or greater. Here we tested the effects of increased mitochondrial antioxidant activity on age-dependent skeletal muscle dysfunction using transgenic mice with targeted overexpression of the human catalase gene to mitochondria (MCat mice). Aged MCat mice exhibited improved voluntary exercise, increased skeletal muscle specific force and tetanic Ca(2+) transients, decreased intracellular Ca(2+) leak and increased sarcoplasmic reticulum (SR) Ca(2+) load compared with age-matched wild type (WT) littermates. Furthermore, ryanodine receptor 1 (the sarcoplasmic reticulum Ca(2+) release channel required for skeletal muscle contraction; RyR1) from aged MCat mice was less oxidized, depleted of the channel stabilizing subunit, calstabin1, and displayed increased single channel open probability (Po). Overall, these data indicate a direct role for mitochondrial free radicals in promoting the pathological intracellular Ca(2+) leak that underlies age-dependent loss of skeletal muscle function. This study harbors implications for the development of novel therapeutic strategies, including mitochondria-targeted antioxidants for treatment of mitochondrial myopathies and other healthspan-limiting disorders.
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Overexpression of mitochondrial-targeted catalase attenuates the effect of ageing on skeletal muscle.
“Furthermore, overexpression of a mitochondrial‐targeted catalase (antioxidant enzyme) has been shown to attenuate the effect of ageing on skeletal muscle, thereby supporting a causal role for mitochondrial dysfunction in the sarcopenic process (Umanskaya et al. 2014).”
From Parkin overexpression protects from ageing‐related loss of muscle mass and strength (2019) · cites this paper as Umanskaya et al. 2014
Overexpression of mitochondrial-targeted catalase attenuates the loss of muscle mass occurring with aging.
“The implication of mitochondrial dysfunction in the sarcopenic process is further supported by the fact that overexpression of the mitochondrial-targeted catalase (an antioxidant enzyme) attenuates the loss of muscle mass occurring with aging (Umanskaya et al., 2014).”
From Effects of Aging and Caloric Restriction on Fiber Type Composition, Mitochondrial Morphology and Dynamics in Rat Oxidative and Glycolytic Muscles (2019) · cites this paper as Umanskaya et al., 2014
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- Authors
- Umanskaya, A., Santulli, G., Xie, W., Andersson, D. C., Reiken, S. R., & Marks, A. R.
- Affiliations
- Columbia University Irving Medical Center (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2014-10-06
- Volume
- 111
- Issue
- 42
- Pages
- 15250-15255
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC4210348
- OpenAlex
- W2146587608
- Cited by
- 157
- References
- 60
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 10 · 2023: 12 · 2022: 8 · 2021: 15 · 2020: 16 · 2019: 13 · 2018: 13 · 2017: 17 · 2016: 21 · 2015: 22 · 2014: 2
- FWCI
- 8.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Columbia Academic Commons (Columbia University)
- Funders
- American Heart Association (AHA13POST16810041, 13POST16810041, 11PRE7810019)
- University of Washington
- National Heart, Lung, and Blood Institute (R01HL061503)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- skeletal muscle aging, catalase overexpression, mitochondrial catalase, sarcoplasmic reticulum calcium, RyR1, mitochondrial free radicals, muscle function, mitochondria-targeted antioxidants, mitochondrial myopathy, transgenic mice
- MeSH terms
- Adenosine Triphosphate, Aging, Animals, Antioxidants, Calcium, Catalase, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Mitochondria, Oxygen, Quality of Life, Sarcoplasmic Reticulum, Stress, Mechanical, Time Factors, Reactive Oxygen Species, Muscle, Skeletal, Ryanodine Receptor Calcium Release Channel, Tacrolimus Binding Protein 1A, Microscopy, Electron, Transmission, Mice
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