ArticleJournal of cell science2014
HDAC1 activates FoxO and is both sufficient and required for skeletal muscle atrophy.
Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.
- Efficacy and safety of probiotics in Parkinson's constipation: A systematic review and meta-analysis.Frontiers in pharmacology · 2022Pooled it
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- Plant‑derived natural products alleviate dexamethasone‑induced skeletal muscle atrophy by modulating FoxO (Review).International journal of molecular medicine · 2026Review
- The Functions and Regulatory Mechanisms of Histone Modifications in Skeletal Muscle Development and Disease.International journal of molecular sciences · 2025Review
- Skeletal Muscle Pathology in Pulmonary Arterial Hypertension and Its Contribution to Exercise Intolerance.Journal of the American Heart Association · 2025Review
- RNA signaling in skeletal muscle: the central role of microRNAs and exosomal microRNAs.Frontiers in cell and developmental biology · 2025Review
- Cancer Cachexia.Advances in experimental medicine and biology · 2025Review
- Muscle Disuse Atrophy.Advances in experimental medicine and biology · 2025Review
- Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024Review
- Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024Review
- The mechanosensitive geneAmerican journal of physiology. Cell physiology · 2024Article
- Fatty infiltration in the musculoskeletal system: pathological mechanisms and clinical implications.Frontiers in endocrinology · 2024Review
- Targeting Epigenetic Regulators with HDAC and BET Inhibitors to Modulate Muscle Wasting.International journal of molecular sciences · 2023Review
- Class I HDAC inhibitors attenuate dexamethasone-induced muscle atrophy via increased protein kinase C (PKC) delta phosphorylation.Cellular signalling · 2023Article
- HDAC8 regulates protein kinase D phosphorylation in skeletal myoblasts in response to stress signaling.Biochemical and biophysical research communications · 2023Article
- The epigenetic regulatory effect of histone acetylation and deacetylation on skeletal muscle metabolism-a review.Frontiers in physiology · 2023Review
- Potential Therapeutic Strategies for Skeletal Muscle Atrophy.Antioxidants (Basel, Switzerland) · 2022Review
- Skeletal Muscle Dysfunction in Experimental Pulmonary Hypertension.International journal of molecular sciences · 2022Article
- Review
- CORP: Gene delivery into murine skeletal muscle using in vivo electroporation.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The Forkhead box O (FoxO) transcription factors are activated, and necessary for the muscle atrophy, in several pathophysiological conditions, including muscle disuse and cancer cachexia. However, the mechanisms that lead to FoxO activation are not well defined. Recent data from our laboratory and others indicate that the activity of FoxO is repressed under basal conditions via reversible lysine acetylation, which becomes compromised during catabolic conditions. Therefore, we aimed to determine how histone deacetylase (HDAC) proteins contribute to activation of FoxO and induction of the muscle atrophy program. Through the use of various pharmacological inhibitors to block HDAC activity, we demonstrate that class I HDACs are key regulators of FoxO and the muscle-atrophy program during both nutrient deprivation and skeletal muscle disuse. Furthermore, we demonstrate, through the use of wild-type and dominant-negative HDAC1 expression plasmids, that HDAC1 is sufficient to activate FoxO and induce muscle fiber atrophy in vivo and is necessary for the atrophy of muscle fibers that is associated with muscle disuse. The ability of HDAC1 to cause muscle atrophy required its deacetylase activity and was linked to the induction of several atrophy genes by HDAC1, including atrogin-1, which required deacetylation of FoxO3a. Moreover, pharmacological inhibition of class I HDACs during muscle disuse, using MS-275, significantly attenuated both disuse muscle fiber atrophy and contractile dysfunction. Together, these data solidify the importance of class I HDACs in the muscle atrophy program and indicate that class I HDAC inhibitors are feasible countermeasures to impede muscle atrophy and weakness.
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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.