The role of raptor in the mechanical load‐induced regulation of mTOR signaling, protein synthesis, and skeletal muscle hypertrophy
Open accessAbstract
It is well known that an increase in mechanical loading can induce skeletal muscle hypertrophy, and a long standing model in the field indicates that mechanical loads induce hypertrophy via a mechanism that requires signaling through the mechanistic target of rapamycin complex 1 (mTORC1). Specifically, it has been widely proposed that mechanical loads activate signaling through mTORC1 and that this, in turn, promotes an increase in the rate of protein synthesis and the subsequent hypertrophic response. However, this model is based on a number of important assumptions that have not been rigorously tested. In this study, we created skeletal muscle specific and inducible raptor knockout mice to eliminate signaling by mTORC1, and with these mice we were able to directly demonstrate that mechanical stimuli can activate signaling by mTORC1, and that mTORC1 is necessary for mechanical load‐induced hypertrophy. Surprisingly, however, we also obtained multiple lines of evidence that indicate that mTORC1 is not required for a mechanical load‐induced increase in the rate of protein synthesis. This observation highlights an important shortcoming in our understanding of how mechanical loads induce hypertrophy and illustrates that additional mTORC1‐independent mechanisms play a critical role in this process.—You, J.‐S., McNally, R. M., Jacobs, B. L., Privett, R. E., Gundermann, D. M., Lin, K.‐H., Steinert, N. D., Goodman, C. A., Hornberger, T. A. The role of raptor in the mechanical load‐induced regulation of mTOR signaling, protein synthesis, and skeletal muscle hypertrophy. FASEB J. 33, 4021–4034 (2019). www.fasebj.org
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Inducible muscle-specific deletion of Raptor blocks muscle hypertrophy but does not blunt the increase of protein synthesis in a mechanical overload model.
“For instance, inducible muscle-specific deletion of Raptor does block muscle hypertrophy but does not blunt the increase of protein synthesis, revealed by puromycin incorporation, in a mechanical overload model13.”
From Mechanisms of muscle atrophy and hypertrophy: implications in health and disease (2021) · cites this paper as [13]
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- Authors
- You, J.-S., Mcnally, R. M., Jacobs, B. L., Privett, R. E., Gundermann, D. M., Lin, K.-H., Steinert, N. D., Goodman, C. A., & Hornberger, T. A.
- Affiliations
- University of Wisconsin–Madison (US)
- Corresponding author
- Hornberger, Troy A.
- ORCID
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2018-12-03
- Volume
- 33
- Issue
- 3
- Pages
- 4021-4034
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- PMC
- PMC6404572
- OpenAlex
- W2902424700
- Cited by
- 149
- References
- 60
- Citations by year
- 2026: 6 · 2025: 13 · 2024: 18 · 2023: 26 · 2022: 19 · 2021: 28 · 2020: 22 · 2019: 14 · 2017: 1
- FWCI
- 5.69
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The FASEB Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Victoria University Research Repository (Victoria University) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR057347)
- 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 › PI3K/AKT/mTOR signaling in cancer
- Keywords
- raptors, mTORC1, skeletal muscle hypertrophy, mechanical loading, protein synthesis, mTOR signaling, muscle-specific knockout
- MeSH terms
- Regulatory-Associated Protein of mTOR, Animals, Physical Exertion, Hypertrophy, Male, Mice, Inbred C57BL, Protein Biosynthesis, Signal Transduction, Muscle, Skeletal, Mice, TOR Serine-Threonine Kinases
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