Regulation of muscle atrophy in aging and disease
Abstract
Muscle aging is characterized by a decline in functional performance and restriction of adaptability, due to progressive loss of muscle tissue coupled with a decrease in strength and force output. Together with selective activation ofapoptotic pathways, a hallmark of age-related muscle loss or sarcopenia is the progressive incapacity of regeneration machinery to replace damaged muscle. These characteristics are shared by pathologies involving muscle wasting, such as muscular dystrophies or amyotrophic lateral sclerosis, cancer and AIDS, all characterized by alterations in metabolic and physiological parameters, progressive weakness in specific muscle groups. Modulation ofextracellular agonists, receptors, protein kinases, intermediate molecules, transcription factors and tissue-specific gene expression collectively compromise the functionality of skeletal muscle tissue, leading to muscle degeneration and persistent protein degradation through activation ofproteolytic systems, such as calpain, ubiquitin-proteasome and caspase. Additional decrements in muscle growth factors compromise skeletal muscle growth, differentiation, survival and regeneration. A better understanding of the mechanisms underlying the pathogenesis of muscle atrophy and wasting associated with different diseases has been the objective of numerous studies and represents an important first step for the development of therapeutic approaches. Among these, insulin-like growth factor-1 (IGF-1) has emerged as a growth factor with a remarkably wide range of actions and a tremendous potential as a therapeutic in attenuating the atrophy and frailty associated with muscle aging and diseases. In this chapter we provide an overview of current concepts in muscle atrophy, focusing specifically on the molecular basis of IGF-1 action and survey current gene and cell therapeutic approaches to rescue muscle atrophy in aging and disease.
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Skeletal muscle mass and function decline with ageing, culminating in sarcopenia, and are linked to an increased burden of senescent cells with involvement of the immune system.
“Skeletal muscle mass and function decline with ageing, culminating in sarcopenia, and are linked to an increased burden of senescent cells with involvement of the immune system.52,53”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [52]
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- Authors
- Vinciguerra, M., Musaro, A., & Rosenthal, N.
- Affiliations
- European Molecular Biology Laboratory (IT)
- Corresponding author
- Vinciguerra, Manlio
- Venue
- Advances in experimental medicine and biology
- Publisher
- Springer US
- Published
- 2010
- Volume
- 694
- Pages
- 211-233
- ISSN
- 0065-2598 (ISSN-L)
- OpenAlex
- W22528786
- Cited by
- 149
- References
- 184
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 3 · 2023: 8 · 2022: 9 · 2021: 8 · 2020: 6 · 2019: 10 · 2018: 12 · 2017: 9 · 2016: 10 · 2015: 12 · 2014: 11 · 2013: 15 · 2012: 15
- FWCI
- 16.78
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Advances in experimental medicine and biology (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- 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 › Physiology › Nutrition and Health in Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Keywords
- muscle atrophy, sarcopenia, muscle aging, insulin-like growth factor I, skeletal muscle regeneration, apoptosis, ubiquitin-proteasome system, calpain, caspases, gene therapy, cell therapy, frailty, muscular dystrophy, amyotrophic lateral sclerosis, cancer cachexia
- MeSH terms
- Aging, Animals, Humans, Muscular Atrophy, Signal Transduction, Muscular Disorders, Atrophic
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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