ArticleThe Journal of biological chemistry2015
Histone deacetylase 6 is a FoxO transcription factor-dependent effector in skeletal muscle atrophy.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- The role and mechanism of histone deacetylase in COPD.Molecular and cellular biochemistry · 2026Review
- Integrated virtual screening, ADMET profiling, and molecular dynamics simulations of novel natural HDAC6 inhibitors with the potential to ameliorate skeletal muscle degeneration.Scientific reports · 2026Article
- NF-κB restrains nutrient-dependent transcription programs through chromatin modulation in Drosophila.Nucleic acids research · 2026Article
- Advanced High-Content Phenotypic Screening to Identify Drugs That Ameliorate the Inhibition of Skeletal Muscle Cell Differentiation Induced by Cancer Cachexia Serum.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Histone deacetylase 6 inhibition promotes microtubule acetylation and facilitates autophagosome-lysosome fusion in dystrophin-deficient mdx mice.Acta physiologica (Oxford, England) · 2025Article
- Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024Review
- Targeting Epigenetic Regulators with HDAC and BET Inhibitors to Modulate Muscle Wasting.International journal of molecular sciences · 2023Review
- HDAC8 regulates protein kinase D phosphorylation in skeletal myoblasts in response to stress signaling.Biochemical and biophysical research communications · 2023Article
- Histone Deacetylases: Molecular Mechanisms and Therapeutic Implications for Muscular Dystrophies.International journal of molecular sciences · 2023Review
- The epigenetic regulatory effect of histone acetylation and deacetylation on skeletal muscle metabolism-a review.Frontiers in physiology · 2023Review
- Genome Editing to Abrogate Muscle Atrophy.Advances in experimental medicine and biology · 2023Review
- Pharmacological inhibition of HDAC6 improves muscle phenotypes in dystrophin-deficient mice by downregulating TGF-β via Smad3 acetylation.Nature communications · 2022Article
- H19 inhibition increases HDAC6 and regulates IRS1 levels and insulin signaling in the skeletal muscle during diabetes.Molecular medicine (Cambridge, Mass.) · 2022Article
- Immunosuppression Induced by Brain-Specific HDAC6 Knockdown Improves Aging Performance inPhenomics (Cham, Switzerland) · 2022Article
- Autophagic LC3Science advances · 2022Article
- Metformin induces muscle atrophy by transcriptional regulation of myostatin via HDAC6 and FoxO3a.Journal of cachexia, sarcopenia and muscle · 2022Article
- Histone deacetylase 6 inhibition restores leptin sensitivity and reduces obesity.Nature metabolism · 2022Article
- Overexpression of Staufen1 in DM1 mouse skeletal muscle exacerbates dystrophic and atrophic features.Human molecular genetics · 2020Article
- Role of Histone Deacetylases in Skeletal Muscle Physiology and Systemic Energy Homeostasis: Implications for Metabolic Diseases and Therapy.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
13 authors at 9 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle atrophy is a severe condition of muscle mass loss. Muscle atrophy is caused by a down-regulation of protein synthesis and by an increase of protein breakdown due to the ubiquitin-proteasome system and autophagy activation. Up-regulation of specific genes, such as the muscle-specific E3 ubiquitin ligase MAFbx, by FoxO transcription factors is essential to initiate muscle protein ubiquitination and degradation during atrophy. HDAC6 is a particular HDAC, which is functionally related to the ubiquitin proteasome system via its ubiquitin binding domain. We show that HDAC6 is up-regulated during muscle atrophy. HDAC6 activation is dependent on the transcription factor FoxO3a, and the inactivation of HDAC6 in mice protects against muscle wasting. HDAC6 is able to interact with MAFbx, a key ubiquitin ligase involved in muscle atrophy. Our findings demonstrate the implication of HDAC6 in skeletal muscle wasting and identify HDAC6 as a new downstream target of FoxO3a in stress response. This work provides new insights in skeletal muscle atrophy development and opens interesting perspectives on HDAC6 as a valuable marker of muscle atrophy and a potential target for pharmacological treatments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.