ArticleThe Journal of clinical investigation2007
Histone deacetylase degradation and MEF2 activation promote the formation of slow-twitch myofibers.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers.
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Who cites it
236 citing papers in PubMed.
- Effect of a session of intensive exercise with ginseng supplementation on histone H3 protein methylation of skeletal muscle of nonathlete men.Molecular genetics & genomic medicine · 2019Trial
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- Skeletal Muscle Effects of GLP 1 Receptor Agonists: Molecular Mechanisms and Comparative Insights on Semaglutide and Tirzepatide, a Narrative Review.International journal of molecular sciences · 2026Review
- The hallmarks of skeletal muscle health.Nature metabolism · 2026Review
- Multi-Omics Insights Into the Mechanisms of Early Muscle Fiber Difference and Transformation Between Lean-Type and Chinese Indigenous Pigs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Changes in palmitate- and stearate-containing glycerophospholipids in skeletal muscle during clenbuterol-induced fast-twitch fiber transition and hypertrophy.The journal of physiological sciences : JPS · 2026Article
- Transient MYC Mimicking the Exercise Response Orchestrates Multifaceted Skeletal Muscle Adaptations.bioRxiv : the preprint server for biology · 2026Article
- ChREBP Is Dispensable for Myofiber Type Switch but Promotes Skeletal Muscle Regeneration.Nutrients · 2026Article
- BRD4 directs myofiber identity and metabolic adaptation through CHD4 cooperation.Nature communications · 2026Article
- Sex- and skeletal muscle-specific gene expression response of histone 3 lysine 27-modifying enzymes by voluntary running in mice.Physiological reports · 2026Article
- Obestatin: canonical and unexpected functions.Reviews in endocrine & metabolic disorders · 2026Review
- Histone deacetylases in Duchenne muscular dystrophy: a role in the mechanism of disease and a target for inhibition.Clinical epigenetics · 2025Review
- Enhancer regulator MLL4 controls skeletal muscle metabolic efficiency by limiting AMPK-mediated fuel catabolism.Nature communications · 2025Article
- Functional Analysis of the mstn1 Gene and Its Transcriptional Regulation by Mef2 Factors in Yellowfin Seabream, Acanthopagrus latus (Hottuyn, 1782).Fish physiology and biochemistry · 2025Article
- The muscle specific MEF2Dα2 isoform promotes muscle ketolysis and running capacity in mice.EMBO reports · 2025Article
- Nuclear CaMKII Isoforms as Regulators of Transcription: From Developmental to Pathological Persistence.Medical sciences (Basel, Switzerland) · 2025Review
- Epigenetic Age Monitoring in Professional Soccer Players for Tracking Recovery and the Effects of Strenuous Exercise.Aging cell · 2025Observational
- Large MAF transcription factors reawaken evolutionarily dormant fast-glycolytic type IIb myofibers in human skeletal muscle.Skeletal muscle · 2025Article
- Histone Deacetylases (HDACs) Roles in Inflammation-mediated Diseases; Current Knowledge.Cell biochemistry and biophysics · 2025Review
- MuSK is a substrate for CaMK2β but this interaction is dispensable for MuSK activation in vivo.Scientific reports · 2025Article
176 more citing papers are in PubMed but not listed here.
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9 authors.
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Abstract
Skeletal muscle is composed of heterogeneous myofibers with distinctive rates of contraction, metabolic properties, and susceptibility to fatigue. We show that class II histone deacetylase (HDAC) proteins, which function as transcriptional repressors of the myocyte enhancer factor 2 (MEF2) transcription factor, fail to accumulate in the soleus, a slow muscle, compared with fast muscles (e.g., white vastus lateralis). Accordingly, pharmacological blockade of proteasome function specifically increases expression of class II HDAC proteins in the soleus in vivo. Using gain- and loss-of-function approaches in mice, we discovered that class II HDAC proteins suppress the formation of slow twitch, oxidative myofibers through the repression of MEF2 activity. Conversely, expression of a hyperactive form of MEF2 in skeletal muscle of transgenic mice promotes the formation of slow fibers and enhances running endurance, enabling mice to run almost twice the distance of WT littermates. Thus, the selective degradation of class II HDACs in slow skeletal muscle provides a mechanism for enhancing physical performance and resistance to fatigue by augmenting the transcriptional activity of MEF2. These findings provide what we believe are new insights into the molecular basis of skeletal muscle function and have important implications for possible therapeutic interventions into muscular diseases.
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