ArticleBMC pharmacology & toxicology2019
Histone deacetylase inhibition by Entinostat for the prevention of electrical and structural remodeling in heart failure.
Article in BMC pharmacology & toxicology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Novel histone deacetylase inhibitor, CS014, attenuates in vivo thrombosis while maintaining hemostasis.Journal of thrombosis and haemostasis : JTH · 2026Article
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- Emerging Epigenetic Therapies for the Treatment of Cardiac Fibrosis.Biomedicines · 2025Review
- Targeting histone deacetylase in cardiac diseases.Frontiers in physiology · 2024Review
- Basic Research Approaches to Evaluate Cardiac Arrhythmia in Heart Failure and Beyond.Frontiers in physiology · 2022Review
- Molecular Mechanisms and Epigenetic Regulation in Diabetic Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Review
- Regulatory Effects of Histone Deacetylase Inhibitors on Myeloid-Derived Suppressor Cells.Frontiers in immunology · 2021Review
- Cardiac contractility modulation attenuates structural and electrical remodeling in a chronic heart failure rabbit model.The Journal of international medical research · 2020Article
- Roles of Histone Acetylation Modifiers and Other Epigenetic Regulators in Vascular Calcification.International journal of molecular sciences · 2020Review
- HDAC inhibition improves cardiopulmonary function in a feline model of diastolic dysfunction.Science translational medicine · 2020Article
- Exploring Molecular Mechanism of Huangqi in Treating Heart Failure Using Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2020Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe development of heart failure is accompanied by complex changes in cardiac electrophysiology and functional properties of cardiomyocytes and fibroblasts. Histone deacetylase (HDAC) inhibitors hold great promise for the pharmaceutical therapy of several malignant diseases. Here, we describe novel effects of the class I HDAC inhibitor Entinostat on electrical and structural remodeling in an in vivo model of pacing induced heart failure.
methodsRabbits were implanted a pacemaker system, subjected to rapid ventricular pacing and treated with Entinostat or placebo, respectively. Following stimulation, rabbit hearts were explanted and subsequently subjected to electrophysiological studies and further immunohistological analyses of left ventricles.
resultsIn vivo, rapid ventricular stimulation caused a significant prolongation of monophasic action potential duration compared to sham hearts (from 173 ± 26 ms to 250 ± 41 ms; cycle length 900 ms; p < 0.05) and an increased incidence of Early afterdepolarisations (+ 150%), while treatment with Entinostat in failing hearts could partially prevent this effect (from 250 ± 41 ms to 170 ± 53 ms, p < 0.05; reduction in EAD by 50%). Entinostat treatment partially restored KCNH2 and Cav1.3 gene expressions in failing hearts, and inhibited the development of cardiac fibrosis in vivo.
conclusionIn a rabbit model of heart failure, Entinostat diminishes heart failure related prolongation of repolarization and partially restores KCNH2 and Cav1.3 expression. In addition, Entinostat exerts antifibrotic properties both in vitro and in vivo. Thus, Entinostat might be an interesting candidate for the pharmaceutical therapy of heart failure directed against structural and electrical remodeling.
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