ArticleCell death & disease2025
Endurance exercise remodels skeletal muscle by suppressing Ythdf1-mediated myostatin expression.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Phase-transition failure in aged skeletal muscle regeneration.Biogerontology · 2026Review
- The role of mNaunyn-Schmiedeberg's archives of pharmacology · 2026Review
- RNA Chemical Modifications in Mammalian Skeletal Muscle Development, Homeostasis, and Disease: Regulatory Mechanisms and Chemical Biology Perspectives.Molecules (Basel, Switzerland) · 2026Review
- Functional Role of ALKBH5 in Kidney Injury: Insights Into Mechanisms and Therapeutic Potential.Journal of cellular biochemistry · 2026Review
- Targeting the activin/myostatin - actrii pathway to preserve skeletal muscle mass in obesity: mechanistic insights and therapeutic perspectives.Reviews in endocrine & metabolic disorders · 2026Review
- Exercise-induced myokines in metabolic regulation: mechanisms, mimetics, and translational potential.Archives of pharmacal research · 2026Review
- Myostatin Research: From Molecular Understanding to Clinical Translation for Musculoskeletal and Metabolic Disorders.International journal of molecular sciences · 2026Review
- TGFβ1-loaded extracellular matrix hydrogels promote skeletal muscle stem cell regeneration via m6A-mediated integrin-ERK signaling.Journal of translational medicine · 2026Article
- Systemic Integrative Mechanisms and Intervention Strategies in Exercise-Induced Skeletal Muscle Damage: Evidence from Animal, Clinical, and Multi-Omics Studies.International journal of molecular sciences · 2026Review
- YTHDC1-Mediated mJournal of agricultural and food chemistry · 2026Article
- Mechanistic interactions of diet, exercise, and pharmacotherapy in skeletal muscle metabolism: evidence and translational perspectives.Frontiers in physiology · 2026Review
- Role of the cGAS-STING signaling pathway in diabetes mellitus and its complications: from mechanisms to therapeutics.Frontiers in pharmacology · 2026Review
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Authors and funding
8 authors.
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Abstract
Exercise can improve health via skeletal muscle remodeling. Elucidating the underlying mechanism may lead to new therapeutics for aging-related loss of skeletal muscle mass. Here, we show that endurance exercise suppresses expression of YT521-B homology domain family (Ythdf1) in skeletal muscle, which recognizes the N6-methyladenosine (m6A). Ythdf1 deletion phenocopies endurance exercise-induced muscle hypertrophy in mice increases muscle mitochondria content and type I fiber specification. At the molecular level, Ythdf1 recognizes and promotes the translation of m6A-modified Mstn mRNA, which encodes a muscle growth inhibitor, Myostatin. Loss of Ythdf1 leads to hyperactivation of skeletal muscle stem cells (MuSCs), also called satellite cells (SCs), enhancing muscle growth and injury-induced regeneration. Our data reveal Ythdf1 as a key regulator of skeletal muscle homeostasis, provide insights into the mechanism by which endurance exercise promotes skeletal muscle remodeling and highlight potential strategies to prevent aging-related muscle degeneration.
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