ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2010
Overexpression of HSP10 in skeletal muscle of transgenic mice prevents the age-related fall in maximum tetanic force generation and muscle Cross-Sectional Area.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- MicroAge mission: experimental design and hardware for a bespoke culture system supporting tissue-engineered skeletal muscle.NPJ microgravity · 2026Article
- Sarcopenia and sepsis fuel a self-perpetuating cycle of immunometabolism decline.Frontiers in immunology · 2026Review
- Redox-regulated signalling of adaptations to contractile activity in skeletal muscle: Implications for age-related muscle weakness.Experimental physiology · 2025Review
- Chaperone Proteins: The Rising Players in Muscle Atrophy.Journal of cachexia, sarcopenia and muscle · 2025Review
- Article
- Heat Shock Proteins: Important Helpers for the Development, Maintenance and Regeneration of Skeletal Muscles.Muscles (Basel, Switzerland) · 2023Review
- Aged gastrocnemius muscle of mice positively responds to a late onset adapted physical training.Frontiers in cell and developmental biology · 2023Article
- Redox Control of Signalling Responses to Contractile Activity and Ageing in Skeletal Muscle.Cells · 2022Review
- Proteins in plasma as a potential biomarkers diagnostic for pelvic organ prolapse.Annals of translational medicine · 2021Article
- On the mechanisms underlying attenuated redox responses to exercise in older individuals: A hypothesis.Free radical biology & medicine · 2020Article
- Hsp90β interacts with MDM2 to suppress p53-dependent senescence during skeletal muscle regeneration.Aging cell · 2019Article
- Aberrant redox signalling and stress response in age-related muscle decline: Role in inter- and intra-cellular signalling.Free radical biology & medicine · 2019Review
- Hsp70 Interacts with Mitogen-Activated Protein Kinase (MAPK)-Activated Protein Kinase 2 To Regulate p38MAPK Stability and Myoblast Differentiation during Skeletal Muscle Regeneration.Molecular and cellular biology · 2018Article
- Therapeutic potential of heat shock protein induction for muscular dystrophy and other muscle wasting conditions.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Review
- The effect of lengthening contractions on neuromuscular junction structure in adult and old mice.Age (Dordrecht, Netherlands) · 2016Article
- Role of reactive oxygen species in age-related neuromuscular deficits.The Journal of physiology · 2016Review
- Redox regulation of muscle adaptations to contractile activity and aging.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Review
- Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression.BioMed research international · 2015Article
- Role of reactive oxygen species in the defective regeneration seen in aging muscle.Free radical biology & medicine · 2013Review
- Mechanisms of skeletal muscle aging: insights from Drosophila and mammalian models.Disease models & mechanisms · 2013Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Skeletal muscle atrophy and weakness are major contributors to frailty and impact significantly on quality of life of older people. Muscle aging is characterized by a loss of maximum tetanic force (P(o)) generation, primarily due to muscle atrophy, to which mitochondrial dysfunction is hypothesized to contribute. We hypothesized that lifelong overexpression of the mitochondrial heat shock protein (HSP) HSP10 in muscle of mice would protect against development of these deficits. P(o) generation by extensor digitorum longus muscles of adult and old wild-type and HSP10-overexpressing mice was determined in situ. Muscles were subjected to damaging lengthening contractions, and force generation was remeasured at 3 h or 28 days to examine susceptibility to, and recovery from, damage, respectively. Muscles of old wild-type mice had a 23% deficit in P(o) generation and a 10% deficit in muscle cross-sectional area compared with muscles of adult wild-type mice. Overexpression of HSP10 prevented this age-related fall in P(o) generation and reduction in cross-sectional area observed in muscles of old wild-type mice. Additionally, overexpression of HSP10 protected against contraction-induced damage independent of age but did not improve recovery if damage occurred. Preservation of muscle force generation and CSA by HSP10 overexpression was associated with protection against the age-related accumulation of protein carbonyls. Data demonstrate that development of age-related muscle weakness may not be inevitable and show, for the first time, that lifelong overexpression of an HSP prevents the age-related loss of P(o) generation. These findings support the hypothesis that mitochondrial dysfunction is involved in the development of age-related muscle deficits.
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Registered trials
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