Cited by 150Muscle Physiology and DisordersCell death mechanisms and regulationNutrition and Health in Aging

Apoptosis in skeletal muscle and its relevance to atrophy

Open access
Dupont-Versteegden, Esther E·2006·World Journal of Gastroenterology

Abstract

Apoptosis is necessary for maintaining the integrity of proliferative tissues, such as epithelial cells of the gastrointestinal system. The role of apoptosis in post mitotic tissues, such as skeletal muscle, is less well defined. Apoptosis during muscle atrophy occurs in both myonuclei and other muscle cell types. Apoptosis of myonuclei likely contributes to the loss of muscle mass, but the mechanisms underlying this process are largely unknown. Caspase-dependent as well as -independent pathways have been implicated and the mode by which atrophy is induced likely determines the apoptotic mechanisms that are utilized. It remains to be determined whether a decrease in apoptosis will alleviate atrophy and distinct research strategies may be required for different causes of skeletal muscle loss.

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Registry

Crossref · 10.3748/wjg.v12.i46.7463

Cites

45 of 45 references verified0 citation errors · 0 not checkable

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  • When triggered in skeletal muscle, apoptosis leads to the loss of one or several myonuclei, thereby decreasing the capacity of a muscle fibre for protein synthesis and, ultimately, leading to fibre atrophy.

    “When triggered in skeletal muscle, apoptosis leads to the loss of one or several myonuclei, thereby decreasing the capacity of a muscle fibre for protein synthesis and, ultimately, leading to fibre atrophy (Dupont‐Versteegden, 2006).”

    From Parkin overexpression protects from ageing‐related loss of muscle mass and strength (2019) · cites this paper as Dupont‐Versteegden, 2006

    The ROLE OF APOPTOSIS section describes each myonucleus as supporting a theoretical amount of cytoplasm, and the paper reports apoptotic myonuclear loss in atrophying muscle. But the Abstract says myonuclear apoptosis *likely* contributes to muscle-mass loss; it does not establish the claimed reduction in protein-synthesis capacity or the definite causal chain to fibre atrophy. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Prolonged activation of apoptosis can result in the loss of muscle fibres.

    “Prolonged activation of apoptosis can even result in the loss of muscle fibres (Dupont‐Versteegden, 2006).”

    From Parkin overexpression protects from ageing‐related loss of muscle mass and strength (2019) · cites this paper as Dupont‐Versteegden, 2006

    The Conclusion links apoptosis to skeletal muscle atrophy, but describes loss of myonuclei and other cells, not loss of whole muscle fibres. The discussion following ROLE OF APOPTOSIS says that eliminating a nucleus does not necessarily destroy the entire muscle cell. Our copy therefore supports a role in atrophy, but not the specific claim that prolonged apoptosis results in fibre loss. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Apoptosis-mediated degradation is associated with aging process of skeletal muscle.

    “Meanwhile, apoptosis-mediated degradation is thought to be associated with the aging process of skeletal muscle [39]”

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Research works printed but not linked: 1

  1. Allen DL, Linderman JK, Roy RR, Grindeland RE, Mukku V, Edgerton VR. Growth hormone/IGF-I and/or resistive e x e r c i s e m a i n t a i n s J Appl Physiol (1985) 1997; 83: 1857-1861

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Authors
Dupont-Versteegden, E. E.
Venue
World Journal of Gastroenterology
Published
2006
Volume
12
Issue
46
Pages
7463
ISSN
1007-9327 (ISSN-L)
OpenAlex
W1540669837
Cited by
150
References
45
Citations by year
2026: 6 · 2025: 12 · 2024: 6 · 2023: 6 · 2022: 10 · 2021: 7 · 2020: 12 · 2019: 5 · 2018: 9 · 2017: 4 · 2016: 6 · 2015: 9 · 2014: 10 · 2013: 5 · 2012: 9
FWCI
0.45
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • World Journal of Gastroenterology (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1r03ag020407-01)
  • National Institute on Aging (AG-20407)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR47577, R01AR047577)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
Keywords
apoptosis, skeletal muscle, muscle atrophy, myonuclei, caspase-dependent apoptosis, caspase-independent apoptosis, muscle mass loss, postmitotic tissues
MeSH terms
Animals, Endodeoxyribonucleases, Humans, Models, Biological, Muscular Atrophy, Apoptosis, Muscle, Skeletal, Proto-Oncogene Proteins c-bcl-2, Caspases, DNA Fragmentation

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