Signalling pathways that mediate skeletal muscle hypertrophy and atrophy
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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PKBα seems to regulate muscle growth.
“PKBα seems to regulate muscle growth [39].”
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Saini, A., Al-Shanti, N., & Stewart, C. (2010) · Cellular Physiology and Biochemistry · doi:10.1159/000276559 · Cited by 12 · see citing works
- Authors
- Glass, D. J.
- Affiliations
- Regeneron (United States) (US)
- Corresponding author
- Glass, David J.
- ORCID
- 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
- Licence
- www.springer.com/tdm (tdm)
- 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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