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Prmt7 Deficiency Causes Reduced Skeletal Muscle Oxidative Metabolism and Age-Related Obesity
Open accessAbstract
Maintenance of skeletal muscle function is critical for metabolic health and the disruption of which exacerbates many chronic diseases such as obesity and diabetes. Skeletal muscle responds to exercise or metabolic demands by a fiber-type switch regulated by signaling-transcription networks that remains to be fully defined. Here, we report that protein arginine methyltransferase 7 (Prmt7) is a key regulator for skeletal muscle oxidative metabolism. Prmt7 is expressed at the highest levels in skeletal muscle and decreased in skeletal muscles with age or obesity. Prmt7(-/-) muscles exhibit decreased oxidative metabolism with decreased expression of genes involved in muscle oxidative metabolism, including PGC-1α. Consistently, Prmt7(-/-) mice exhibited significantly reduced endurance exercise capacities. Furthermore, Prmt7(-/-) mice exhibit decreased energy expenditure, which might contribute to the exacerbated age-related obesity of Prmt7(-/-) mice. Similarly to Prmt7(-/-) muscles, Prmt7 depletion in myoblasts also reduces PGC-1α expression and PGC-1α-promoter driven reporter activities. Prmt7 regulates PGC-1α expression through interaction with and activation of p38 mitogen-activated protein kinase (p38MAPK), which in turn activates ATF2, an upstream transcriptional activator for PGC-1α. Taken together, Prmt7 is a novel regulator for muscle oxidative metabolism via activation of p38MAPK/ATF2/PGC-1α.
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“Prmt7 modulates PGC-1α expression via interaction with and activation of p38MAPK [12].”
From Apigenin Enhances Skeletal Muscle Hypertrophy and Myoblast Differentiation by Regulating Prmt7 (2017) · cites this paper as [12]
In the citing paper
“PGC-1α expression was attenuated by Prmt7 knockdown, consistent with a previous study [12].”
From Apigenin Enhances Skeletal Muscle Hypertrophy and Myoblast Differentiation by Regulating Prmt7 (2017) · cites this paper as [12]
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“A previous study has shown that knockdown of Prmt7 reduces MHC and myogenin expression, as well as p38 phosphorylation [12].”
From Apigenin Enhances Skeletal Muscle Hypertrophy and Myoblast Differentiation by Regulating Prmt7 (2017) · cites this paper as [12]
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Metadata
- Authors
- Jeong, H.-J., Lee, H.-J., Vuong, T. A., Choi, K.-S., Choi, D., Koo, S.-H., Cho, S. C., Cho, H., & Kang, J.-S.
- Affiliations
- Samsung Biomedical Research Institute (KR)
- Samsung (South Korea) (KR)
- Korea University (KR)
- Corresponding author
- Kang, Jong-Sun
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2016-04-26
- Volume
- 65
- Issue
- 7
- Pages
- 1868-1882
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2342571247
- Cited by
- 101
- References
- 55
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 10 · 2023: 9 · 2022: 12 · 2021: 11 · 2020: 11 · 2019: 16 · 2018: 8 · 2017: 8 · 2016: 1
- FWCI
- 5.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Research Foundation of Korea (NRF-2011-0017315, NRF-2013M3A9B1069776)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer-related gene regulation
- Keywords
- PRMT7, skeletal muscle oxidative metabolism, age-related obesity, PGC-1α, p38 MAPK, ATF2, endurance exercise capacity, energy expenditure, myoblasts, muscle fiber type shift, transcriptional regulation
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Aging, Animals, Energy Metabolism, Female, Lipids, Male, Obesity, Oxygen Consumption, Physical Conditioning, Animal, Physical Endurance, Promoter Regions, Genetic, Protein-Arginine N-Methyltransferases, Signal Transduction, Mice, Knockout, Muscle, Skeletal, Myoblasts, Mice, Activating Transcription Factor 2
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