ArticleThe Journal of pharmacology and experimental therapeutics2016
Class I Histone Deacetylase Inhibition for the Treatment of Sustained Atrial Fibrillation.
Article in The Journal of pharmacology and experimental therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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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
21 citing papers in PubMed, 37 citations in OpenAlex.
- Integrated bioinformatics and clinical validation of oxidative stress-associated genes in atrial fibrillation and chronic kidney disease.Experimental and therapeutic medicine · 2026Article
- Epigenetics in Atrial Fibrillation: Molecular Mechanisms and Therapeutic Avenues.Reviews in cardiovascular medicine · 2026Review
- Epigenetic Liquid Biopsy Marks Atrial Fibrillation: Evidence from the AF Big Picture Study.Epigenomes · 2026Article
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- Lysine 2-hydroxyisobutyrylation of HXK1 alters energy metabolism and KCell communication and signaling : CCS · 2025Article
- Epigenetic Regulation in Myocardial Fibroblasts and Its Impact on Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Review
- Classification models and SAR analysis on HDAC1 inhibitors using machine learning methods.Molecular diversity · 2023Article
- Differential regulation of KPhysiological reports · 2021Article
- Epigenetics in atrial fibrillation: A reappraisal.Heart rhythm · 2021Review
- Epigenetic regulation of cardiac electrophysiology in atrial fibrillation: HDAC2 determines action potential duration and suppresses NRSF in cardiomyocytes.Basic research in cardiology · 2021Article
- Epigenetic Mechanism and Therapeutic Implications of Atrial Fibrillation.Frontiers in cardiovascular medicine · 2021Review
- Histone Deacetylases in the Pathogenesis of Diabetic Cardiomyopathy.Frontiers in endocrinology · 2021Review
- Genetics and Epigenetics of Atrial Fibrillation.International journal of molecular sciences · 2020Review
- PROTAC-mediated degradation of class I histone deacetylase enzymes in corepressor complexes.Chemical communications (Cambridge, England) · 2020Article
- Atrogin-1/MAFbx mRNA expression is regulated by histone deacetylase 1 in rat soleus muscle under hindlimb unloading.Scientific reports · 2019Article
- Article
- HDAC Inhibitors: Therapeutic Potential in Fibrosis-Associated Human Diseases.International journal of molecular sciences · 2019Review
- HDAC (Histone Deacetylase) Inhibitor Valproic Acid Attenuates Atrial Remodeling and Delays the Onset of Atrial Fibrillation in Mice.Circulation. Arrhythmia and electrophysiology · 2019Article
- HDAC inhibitors as antifibrotic drugs in cardiac and pulmonary fibrosis.Therapeutic advances in chronic disease · 2019Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
Current therapies are less effective for treating sustained/permanent versus paroxysmal atrial fibrillation (AF). We and others have previously shown that histone deacetylase (HDAC) inhibition reverses structural and electrical atrial remodeling in mice with inducible, paroxysmal-like AF. Here, we hypothesize an important, specific role for class I HDACs in determining structural atrial alterations during sustained AF. The class I HDAC inhibitor N-acetyldinaline [4-(acetylamino)-N-(2-amino-phenyl) benzamide] (CI-994) was administered for 2 weeks (1 mg/kg/day) to Hopx transgenic mice with atrial remodeling and inducible AF and to dogs with atrial tachypacing-induced sustained AF. Class I HDAC inhibition prevented atrial fibrosis and arrhythmia inducibility in mice. Dogs were divided into three groups: 1) sinus rhythm, 2) sustained AF plus vehicle, and 3) sustained AF plus CI-994. In group 3, the time in AF over 2 weeks was reduced by 30% compared with group 2, along with attenuated atrial fibrosis and intra-atrial adipocyte infiltration. Moreover, group 2 dogs had higher atrial and serum inflammatory cytokines, adipokines, and atrial immune cells and adipocytes compared with groups 1 and 3. On the other hand, groups 2 and 3 displayed similar left atrial size, ventricular function, and mitral regurgitation. Importantly, the same histologic alterations found in dogs with sustained AF and reversed by CI-994 were also present in atrial tissue from transplanted patients with chronic AF. This is the first evidence that, in sustained AF, class I HDAC inhibition can reduce the total time of fibrillation, atrial fibrosis, intra-atrial adipocytes, and immune cell infiltration without significant effects on cardiac function.
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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.