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Localized Igf-1 transgene expression sustains hypertrophy and regeneration in senescent skeletal muscle
Abstract
Aging skeletal muscles suffer a steady decline in mass and functional performance, and compromised muscle integrity as fibrotic invasions replace contractile tissue, accompanied by a characteristic loss in the fastest, most powerful muscle fibers. The same programmed deficits in muscle structure and function are found in numerous neurodegenerative syndromes and disease-related cachexia. We have generated a model of persistent, functional myocyte hypertrophy using a tissue-restricted transgene encoding a locally acting isoform of insulin-like growth factor-1 that is expressed in skeletal muscle (mIgf-1). Transgenic embryos developed normally, and postnatal increases in muscle mass and strength were not accompanied by the additional pathological changes seen in other Igf-1 transgenic models. Expression of GATA-2, a transcription factor normally undetected in skeletal muscle, marked hypertrophic myocytes that escaped age-related muscle atrophy and retained the proliferative response to muscle injury characteristic of younger animals. The preservation of muscle architecture and age-independent regenerative capacity through localized mIgf-1 transgene expression suggests clinical strategies for the treatment of age or disease-related muscle frailty.
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“Muscle-specific overexpression of a locally acting IGF1 isoform in mice showed that localized IGF1 expression sustains muscle growth and regeneration6.”
From Mechanisms of muscle atrophy and hypertrophy: implications in health and disease (2021) · cites this paper as [6]
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Metadata
- Authors
- Musarò, A., McCullagh, K., Paul, A., Houghton, L., Dobrowolny, G., Molinaro, M., Barton, E. R., L Sweeney, H., & Rosenthal, N.
- Affiliations
- Massachusetts General Hospital (US)
- Sapienza University of Rome (IT)
- University of Pennsylvania (US)
- Corresponding author
- Rosenthal, Nadia
- ORCID
- Venue
- Nature Genetics
- Published
- 2001-02
- Volume
- 27
- Issue
- 2
- Pages
- 195-200
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- OpenAlex
- W1562705858
- Cited by
- 1,137
- References
- 30
- Citations by year
- 2026: 17 · 2025: 19 · 2024: 27 · 2023: 22 · 2022: 21 · 2021: 27 · 2020: 29 · 2019: 35 · 2018: 38 · 2017: 28 · 2016: 34 · 2015: 60 · 2014: 52 · 2013: 59 · 2012: 71
- FWCI
- 17.57
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Genetics (clinical) › Neurogenetic and Muscular Disorders Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Physical Performance
- Keywords
- insulin-like growth factor I, skeletal muscle aging, muscle atrophy, myocyte hypertrophy, muscle regeneration, muscle fibrosis, GATA2, transgenic mouse model, muscle strength
- MeSH terms
- Animals, Cachexia, DNA-Binding Proteins, Hypertrophy, Insulin-Like Growth Factor I, Mice, Transgenic, Organ Size, Regeneration, Tissue Distribution, Transcription Factors, Cellular Senescence, Muscle, Skeletal, Neurodegenerative Diseases, Protein Isoforms, GATA2 Transcription Factor, Mice
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