Cited by 694Muscle Physiology and DisordersMuscle metabolism and nutritionMetabolism, Diabetes, and Cancer

Signalling pathways that mediate skeletal muscle hypertrophy and atrophy

Glass, David J.·2003·Nature Cell Biology

Abstract

Atrophy of skeletal muscle is a serious consequence of numerous diseases, including cancer and AIDS. Successful treatments for skeletal muscle atrophy could either block protein degradation pathways activated during atrophy or stimulate protein synthesis pathways induced during skeletal muscle hypertrophy. This perspective will focus on the signalling pathways that control skeletal muscle atrophy and hypertrophy, including the recently identified ubiquitin ligases muscle RING finger 1 (MuRF1) and muscle atrophy F-box (MAFbx), as a basis to develop targets for pharmacologic intervention in muscle disease.

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Crossref · 10.1038/ncb0203-87

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Authors
Glass, D. J.
Affiliations
Regeneron (United States) (US)
Corresponding author
Glass, David J.
Venue
Nature Cell Biology
Published
2003-02
Volume
5
Issue
2
Pages
87-90
ISSN
  • 1465-7392 (ISSN-L)
  • 1476-4679
OpenAlex
W1965044262
Cited by
694
References
52
Citations by year
2026: 11 · 2025: 14 · 2024: 25 · 2023: 21 · 2022: 27 · 2021: 25 · 2020: 22 · 2019: 22 · 2018: 31 · 2017: 23 · 2016: 36 · 2015: 32 · 2014: 34 · 2013: 38 · 2012: 34
FWCI
3.01
Type
journal article
Language
en
Open access
closed
Locations
  • Nature Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Procter and Gamble
  • Regeneron Pharmaceuticals
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
skeletal muscle atrophy, skeletal muscle hypertrophy, signaling pathways, protein degradation, protein synthesis, ubiquitin ligase, MuRF1, atrogin-1, cancer cachexia, pharmacological interventions
MeSH terms
Tripartite Motif Proteins, Animals, Humans, Hypertrophy, Insulin-Like Growth Factor I, Ligases, Muscle Proteins, Muscular Atrophy, Proto-Oncogene Proteins, Signal Transduction, Protein Serine-Threonine Kinases, Receptors, Adrenergic, beta-2, Muscle, Skeletal, Calcineurin, Phosphatidylinositol 3-Kinases, Ubiquitin-Protein Ligases, SKP Cullin F-Box Protein Ligases, Proto-Oncogene Proteins c-akt

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