ArticleAmerican journal of physiology. Heart and circulatory physiology2014
HDAC6 contributes to pathological responses of heart and skeletal muscle to chronic angiotensin-II signaling.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 121 citations in OpenAlex.
- HDAC inhibition via suberoylanilide hydroxamic acid ameliorates doxorubicin-induced cardiotoxicity.Nature communications · 2026Article
- Mechanisms of Atrial Fibrillation in Heart Failure: Uncovering Therapeutic Targets in the Atrial Substrate.Current heart failure reports · 2026Review
- Interconnected Pathways and Therapeutic Implications for Cardiovascular Aging and Diseases.JACC. Asia · 2026Review
- HDACs and Their Inhibitors on Post-Translational Modifications: The Regulation of Cardiovascular Disease.Cells · 2025Review
- The role of HDAC6 in fibrosis: a novel and effective therapy strategy.European journal of medical research · 2025Review
- Enzyme-independent functions of HDAC3 in the adult heart.Acta pharmaceutica Sinica. B · 2025Article
- Myocardial transcriptomic and proteomic landscapes across the menopausal continuum in a murine model of chemically induced accelerated ovarian failure.Physiological genomics · 2025Article
- Genetic deletion or pharmacologic inhibition of histone deacetylase 6 protects the heart against ischaemia/reperfusion injury by limiting tumour necrosis factor alpha-induced mitochondrial injury in experimental diabetes.Cardiovascular research · 2024Article
- Chronic kidney disease activates the HDAC6-inflammatory axis in the heart and contributes to myocardial remodeling in mice: inhibition of HDAC6 alleviates chronic kidney disease-induced myocardial remodeling.Basic research in cardiology · 2024Article
- Histone deacetylase 6 controls cardiac fibrosis and remodelling through the modulation of TGF-β1/Smad2/3 signalling in post-infarction mice.Journal of cellular and molecular medicine · 2024Article
- Histone deacetylase 6 as a novel promising target to treat cardiovascular disease.Cancer innovation · 2024Review
- Targeting histone deacetylase in cardiac diseases.Frontiers in physiology · 2024Review
- Novel Therapeutic Avenues for Hypertrophic Cardiomyopathy.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023Review
- Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023Review
- Knockdown of HDAC6 alleviates ventricular remodeling in experimental dilated cardiomyopathy via inhibition of NLRP3 inflammasome activation and promotion of cardiomyocyte autophagy.Cell biology and toxicology · 2023Article
- The Role of Selected Epigenetic Pathways in Cardiovascular Diseases as a Potential Therapeutic Target.International journal of molecular sciences · 2023Review
- HDAC6 Deficiency Has Moderate Effects on Behaviors and Parkinson's Disease Pathology in Mice.International journal of molecular sciences · 2023Article
- Advances in the Mechanistic Study of the Control of Oxidative Stress Injury by Modulating HDAC6 Activity.Cell biochemistry and biophysics · 2023Article
- Roles of histone acetylation sites in cardiac hypertrophy and heart failure.Frontiers in cardiovascular medicine · 2023Review
- Histone Deacetylase 6 Inhibitor JS28 Prevents Pathological Gene Expression in Cardiac Myocytes.Journal of the American Heart Association · 2022Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
Little is known about the function of the cytoplasmic histone deacetylase HDAC6 in striated muscle. Here, we addressed the role of HDAC6 in cardiac and skeletal muscle remodeling induced by the peptide hormone angiotensin II (ANG II), which plays a central role in blood pressure control, heart failure, and associated skeletal muscle wasting. Comparable with wild-type (WT) mice, HDAC6 null mice developed cardiac hypertrophy and fibrosis in response to ANG II. However, whereas WT mice developed systolic dysfunction upon treatment with ANG II, cardiac function was maintained in HDAC6 null mice treated with ANG II for up to 8 wk. The cardioprotective effect of HDAC6 deletion was mimicked in WT mice treated with the small molecule HDAC6 inhibitor tubastatin A. HDAC6 null mice also exhibited improved left ventricular function in the setting of pressure overload mediated by transverse aortic constriction. HDAC6 inhibition appeared to preserve systolic function, in part, by enhancing cooperativity of myofibrillar force generation. Finally, we show that HDAC6 null mice are resistant to skeletal muscle wasting mediated by chronic ANG-II signaling. These findings define novel roles for HDAC6 in striated muscle and suggest potential for HDAC6-selective inhibitors for the treatment of cardiac dysfunction and muscle wasting in patients with heart failure.
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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.