ArticleMolecular biology of the cell2009
A histone deacetylase 4/myogenin positive feedback loop coordinates denervation-dependent gene induction and suppression.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.
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Who cites it
82 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.
- Identification of potential microRNAs and KEGG pathways in denervation muscle atrophy based on meta-analysis.Scientific reports · 2021Pooled it
- Neuromuscular magnetic stimulation counteracts muscle decline in ALS patients: results of a randomized, double-blind, controlled study.Scientific reports · 2019Trial
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- Global MyoG research 2004-2024: a bibliometric analysis of trends and translational implications.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- GW8510 alleviates muscle atrophy and skeletal muscle dysfunction in mice through AMPK/PGC1α signaling.International journal of molecular medicine · 2025Article
- Article
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- The Role of Non-Coding RNAs in ALS.Genes · 2025Review
- MuSK is a substrate for CaMK2β but this interaction is dispensable for MuSK activation in vivo.Scientific reports · 2025Article
- Single-nuclei sequencing of skeletal muscle reveals subsynaptic-specific transcripts involved in neuromuscular junction maintenance.Nature communications · 2025Article
- Muscle-specific kinase levels in blood are an early diagnostic biomarker for SOD1-93A mouse model of ALS.Frontiers in neurology · 2025Article
- Skeletal muscle reprogramming enhances reinnervation after peripheral nerve injury.Nature communications · 2024Article
- CaMKIIβ deregulation contributes to neuromuscular junction destabilization in Myotonic Dystrophy type I.Skeletal muscle · 2024Article
- MiR206 and 423-3p Are Differently Modulated in Fast and Slow-Progressing Amyotrophic Lateral Sclerosis Patients.Neuromolecular medicine · 2024Article
- Skeletal muscle reprogramming enhances reinnervation after peripheral nerve injury.Research square · 2024Article
- Identification of a muscle-specific isoform of VMA21 as a potent actor in X-linked myopathy with excessive autophagy pathogenesis.Human molecular genetics · 2023Article
- Sodium butyrate does not protect spinal motor neurons from AMPA-induced excitotoxic degeneration in vivo.Disease models & mechanisms · 2023Article
- Skeletal Muscle Denervation: Past, Present and Future.International journal of molecular sciences · 2022Article
- Supraphysiological activation of TAK1 promotes skeletal muscle growth and mitigates neurogenic atrophy.Nature communications · 2022Article
- Non-coding RNA in rhabdomyosarcoma progression and metastasis.Frontiers in oncology · 2022Review
22 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Muscle activity contributes to formation of the neuromuscular junction and affects muscle metabolism and contractile properties through regulated gene expression. However, the mechanisms coordinating these diverse activity-regulated processes remain poorly characterized. Recently, it was reported that histone deacetylase 4 (HDAC4) can mediate denervation-induced myogenin and nicotinic acetylcholine receptor gene expression. Here, we report that HDAC4 is not only necessary for denervation-dependent induction of genes involved in synaptogenesis (nicotinic acetylcholine receptor and muscle-specific receptor tyrosine kinase) but also for denervation-dependent suppression of genes involved in glycolysis (muscle-specific enolase and phosphofructokinase). In addition, HDAC4 differentially regulates genes involved in muscle fiber type specification by inducing myosin heavy chain IIA and suppressing myosin heavy chain IIB. Consistent with these regulated gene profiles, HDAC4 is enriched in fast oxidative fibers of innervated tibialis anterior muscle and HDAC4 knockdown enhances glycolysis in cultured myotubes. HDAC4 mediates gene induction indirectly by suppressing the expression of Dach2 and MITR that function as myogenin gene corepressors. In contrast, HDAC4 is directly recruited to myocyte enhancer factor 2 sites within target promoters to mediate gene suppression. Finally, we discovered an HDAC4/myogenin positive feedback loop that coordinates gene induction and repression underlying muscle phenotypic changes after muscle denervation.
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