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Cited by 1,583Muscle Physiology and DisordersMuscle metabolism and nutritionSignaling Pathways in Disease

The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.

Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathways

Rommel, Christian, Bodine, Sue C., Clarke, Brian A., Rossman, Roni, Nunez, Lorna, Stitt, Trevor N., Yancopoulos, George D., Glass, David J.·2001·Nature Cell Biology
DOI 10.1038/ncb1101-1009
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Abstract

Skeletal muscle is composed of multinucleated fibres, formed after the differentiation and fusion of myoblast precursors. Skeletal muscle atrophy and hypertrophy refer to changes in the diameter of these pre-existing muscle fibres. The prevention of atrophy would provide an obvious clinical benefit; insulin-like growth factor 1 (IGF-1) is a promising anti-atrophy agent because of its ability to promote hypertrophy. However, the signalling pathways by which IGF-1 promotes hypertrophy remain unclear, with roles suggested for both the calcineurin/NFAT (nuclear factor of activated T cells) pathway and the PtdIns-3-OH kinase (PI(3)K)/Akt pathway. Here we employ a battery of approaches to examine these pathways during the hypertrophic response of cultured myotubes to IGF-1. We report that Akt promotes hypertrophy by activating downstream signalling pathways previously implicated in activating protein synthesis: the pathways downstream of mammalian target of rapamycin (mTOR) and the pathway activated by phosphorylating and thereby inhibiting glycogen synthase kinase 3 (GSK3). In contrast, in addition to demonstrating that calcineurin does not mediate IGF-1-induced hypertrophy, we show that IGF-1 unexpectedly acts via Akt to antagonize calcineurin signalling during myotube hypertrophy.

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Research works printed but not linked: 3

  1. Engel, A. G. & Fanzine-Armstrong, C. Myology 1937 (McGraw-Hill, New York, 1994).
  2. Florini, J. R., Ewton, D. Z. & Coolican, S. A. Endocr. Rev. 17, 481–517 (1996).
  3. Yu, H. & Berkel, H. J. LA State Med. Soc. 151, 218–223 (1999).

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Metadata

Authors
Rommel, C., Bodine, S. C., Clarke, B. A., Rossman, R., Nunez, L., Stitt, T. N., Yancopoulos, G. D., & Glass, D. J.
Affiliations
Regeneron (United States) (US)
Corresponding author
Glass, David J.
ORCID
Venue
Nature Cell Biology
Publisher
Springer Science and Business Media LLC
Published
2001-10-05
Volume
3
Issue
11
Pages
1009-1013
ISSN
  • 1465-7392 (ISSN-L)
  • 1476-4679
DOI
10.1038/ncb1101-1009
OpenAlex
W1530473805
Cited by
1,583
References
24
Citations by year
2026: 29 · 2025: 37 · 2024: 60 · 2023: 48 · 2022: 73 · 2021: 72 · 2020: 60 · 2019: 63 · 2018: 75 · 2017: 68 · 2016: 71 · 2015: 78 · 2014: 82 · 2013: 107 · 2012: 101
FWCI
12.69
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Regeneron Pharmaceuticals
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
insulin-like growth factor I, skeletal muscle hypertrophy, myotubes, PI3K/Akt signaling, mTOR, glycogen synthase kinase-3, calcineurin, NFAT, muscle atrophy, protein synthesis
MeSH terms
Phosphoinositide-3 Kinase Inhibitors, Animals, Carrier Proteins, Cell Differentiation, Cell Line, Insulin-Like Growth Factor I, Muscular Atrophy, Phosphoproteins, Phosphorylation, Protein Kinases, Proto-Oncogene Proteins, Signal Transduction, Protein Serine-Threonine Kinases, Calcium-Calmodulin-Dependent Protein Kinases, Muscle, Skeletal, Cell Cycle Proteins, Calcineurin, Phosphatidylinositol 3-Kinases, Ribosomal Protein S6 Kinases, Glycogen Synthase Kinases, Glycogen Synthase Kinase 3, Eukaryotic Initiation Factors, Protein Kinase Inhibitors, Adaptor Proteins, Signal Transducing, Proto-Oncogene Proteins c-akt, Mice, TOR Serine-Threonine Kinases

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