ArticleCellular & molecular biology letters2024
Exercise promotes skeletal muscle growth in adolescents via modulating Mettl3-mediated m6A methylation of MyoD in muscle satellite cells.
Article in Cellular & molecular biology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Review
- RNA Chemical Modifications in Mammalian Skeletal Muscle Development, Homeostasis, and Disease: Regulatory Mechanisms and Chemical Biology Perspectives.Molecules (Basel, Switzerland) · 2026Review
- The role of mNaunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Resistance-based exercise restores muscle health in dialysis patients.Journal of muscle research and cell motility · 2026Article
- Astragaloside IV Suppresses Gastric Cancer by m6A-dependent FSP1 Modulation and Ferroptosis Induction.Biological procedures online · 2026Article
- YTHDC1-Mediated mJournal of agricultural and food chemistry · 2026Article
- m6A modification on ncRNAs and underlying mechanisms of exercise in the regulation of pathological cardiac remodeling.European journal of medical research · 2025Review
- Article
- Oestrogen suppresses the adipogenesis of fibro/adipogenic progenitors through reactivating the METTL3-ESR1-mediated loop in post-menopausal females.Clinical and translational medicine · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundExercise exerts positive impacts on skeletal muscle health and homeostasis. Emerging evidence suggests that m6A methylation is involved in various physiological processes. However, the impact of exercise on adolescent skeletal muscle growth and the underlying epigenetic mechanisms remain poorly understood.
methodsThe lower-limb skeletal muscles were harvested from exercise and control groups to compare the skeletal muscle growth in adolescents. mRNA sequencing was conducted to explore the mechanisms underlying enhanced skeletal muscle growth following exercise. The effects and mechanisms of Mettl3-mediated m6A methylation on adolescent skeletal muscle growth were investigated using muscle satellite cell (MuSC)-specific Mettl3 knockout (KO) mice. The potential function of MyoD for skeletal muscle growth in adolescents was explored by phenotypes after overexpression and evaluation of in vivo myogenesis. Additionally, the effects of the methyl donor betaine on adolescent skeletal muscle growth were investigated in vitro and in vivo.
resultsExercise could promote skeletal muscle growth in adolescents. Sequencing data analysis and confirmation assays uncovered that exercise significantly increased Mettl3-mediated m6A methylation and elevated the expression levels of activation marker MyoD in MuSCs. Establishment of MuSC-specific Mettl3 KO mice further demonstrated that Mettl3-mediated m6A methylation in MyoD contributed to skeletal muscle growth during adolescence. Mettl3-mediated m6A methylation regulated MyoD mRNA stability at the posttranscriptional level in MuSCs, with a functional site at 234 bp A. Increased expression of MyoD could contribute to myogenesis of adolescent MuSCs. Furthermore, the methyl donor betaine could enhance MyoD expression, contributing to MuSCs activation and skeletal muscle growth in adolescents by boosting m6A methylation levels.
conclusionsExercise promoted skeletal muscle growth in adolescents through facilitating MyoD mRNA stability of MuSCs in a Mettl3-mediated m6A-dependent manner. The methyl donor betaine could be a potential alternative to exercise for promoting adolescent skeletal muscle growth by directly augmenting the global levels of m6A methylation. These findings may provide a theoretical foundation for encouraging daily fitness exercise and ensuring healthy growth in adolescents.
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