Cited by 149Muscle Physiology and DisordersNutrition and Health in AgingMuscle metabolism and nutrition

Regulation of muscle atrophy in aging and disease

Vinciguerra, Manlio, Musaro, Antonio, Rosenthal, Nadia·2010·Advances in experimental medicine and biology

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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Crossref · 10.1007/978-1-4419-7002-2_15

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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

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