JunB transcription factor maintains skeletal muscle mass and promotes hypertrophy
Open accessAbstract
The size of skeletal muscle cells is precisely regulated by intracellular signaling networks that determine the balance between overall rates of protein synthesis and degradation. Myofiber growth and protein synthesis are stimulated by the IGF-1/Akt/mammalian target of rapamycin (mTOR) pathway. In this study, we show that the transcription factor JunB is also a major determinant of whether adult muscles grow or atrophy. We found that in atrophying myotubes, JunB is excluded from the nucleus and that decreasing JunB expression by RNA interference in adult muscles causes atrophy. Furthermore, JunB overexpression induces hypertrophy without affecting satellite cell proliferation and stimulated protein synthesis independently of the Akt/mTOR pathway. When JunB is transfected into denervated muscles, fiber atrophy is prevented. JunB blocks FoxO3 binding to atrogin-1 and MuRF-1 promoters and thus reduces protein breakdown. Therefore, JunB is important not only in dividing populations but also in adult muscle, where it is required for the maintenance of muscle size and can induce rapid hypertrophy and block atrophy.
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JunB, PGC1α, and PGC1β inhibit FoxO activity in skeletal muscles, while the glucocorticoid receptor and β-catenin synergize with FoxOs to promote muscle wasting.
“For instance, JunB, PGC1α, and PGC1β all inhibit FoxO activity in skeletal muscles2,67,68, while the glucocorticoid receptor and β−catenin synergize with FoxOs to promote muscle wasting69.”
From Mechanisms of muscle atrophy and hypertrophy: implications in health and disease (2021) · cites this paper as [68]
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- Authors
- Raffaello, A., Milan, G., Masiero, E., Carnio, S., Lee, D., Lanfranchi, G., Goldberg, A. L., & Sandri, M.
- Affiliations
- Harvard University (US)
- Veneto Institute of Molecular Medicine (IT)
- University of Padua (IT)
- Corresponding author
- Lanfranchi, Gerolamo
- Sandri, Marco
- ORCID
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2010-10-04
- Volume
- 191
- Issue
- 1
- Pages
- 101-113
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2953439
- OpenAlex
- W2014897682
- Cited by
- 156
- References
- 50
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 11 · 2023: 6 · 2022: 11 · 2021: 14 · 2020: 15 · 2019: 9 · 2018: 10 · 2017: 8 · 2016: 6 · 2015: 10 · 2014: 11 · 2013: 12 · 2012: 12
- FWCI
- 4.43
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Padua Research Archive (University of Padova) (submittedVersion, cc-by-nc-sa)
- 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 › Agricultural and Biological Sciences › Animal Science and Zoology › Meat and Animal Product Quality
- Keywords
- skeletal muscle hypertrophy, muscle atrophy, FOXO3, atrogin-1, MuRF1, protein degradation, protein synthesis, Akt/mTOR signaling, denervation, satellite cells, myofiber growth, muscle mass preservation
- MeSH terms
- Tripartite Motif Proteins, Forkhead Box Protein O3, Animals, Hypertrophy, Muscle Proteins, Muscular Atrophy, Promoter Regions, Genetic, Protein Biosynthesis, Signal Transduction, Proto-Oncogene Proteins c-jun, Muscle, Skeletal, Muscle Fibers, Skeletal, Ubiquitin-Protein Ligases, SKP Cullin F-Box Protein Ligases, Mice, Forkhead Transcription Factors
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