ArticleCell & bioscience2021
The crosstalk of HDAC3, microRNA-18a and ADRB3 in the progression of heart failure.
Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 23 citations in OpenAlex.
- Impact of left ventricular ejection fraction on unplanned readmission after aortic regurgitation surgery: a single-center retrospective cohort study.Frontiers in cardiovascular medicine · 2026Article
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Correlations of serum histone deacetylase 3 and thrombospondin-1 levels with cardiac function grades, ventricular remodeling, and prognosis in patients with chronic heart failure.Journal of cardiothoracic surgery · 2025Article
- Targeting histone deacetylase in cardiac diseases.Frontiers in physiology · 2024Review
- Unique miRomics Expression Profiles inInternational journal of molecular sciences · 2023Article
- Article
- TFRC in cardiomyocytes promotes macrophage infiltration and activation during the process of heart failure through regulating Ccl2 expression mediated by hypoxia inducible factor-1α.Immunity, inflammation and disease · 2023Article
- Review
- The role of HDAC3 and its inhibitors in regulation of oxidative stress and chronic diseases.Cell death discovery · 2023Review
- Identification of novel leads as potent inhibitors of HDAC3 using ligand-based pharmacophore modeling and MD simulation.Scientific reports · 2022Article
- Identification of energy metabolism-related biomarkers for risk prediction of heart failure patients using random forest algorithm.Frontiers in cardiovascular medicine · 2022Article
- Expression and Regulation Network of HDAC3 in Acute Myeloid Leukemia and the Implication for Targeted Therapy Based on Multidataset Data Mining.Computational and mathematical methods in medicine · 2022Article
- The critical roles of histone deacetylase 3 in the pathogenesis of solid organ injury.Cell death & disease · 2021Review
- MiR-29a Increase in Aging May Function as a Compensatory Mechanism Against Cardiac Fibrosis Through SERPINH1 Downregulation.Frontiers in cardiovascular medicine · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHeart failure (HF) is a clinical syndrome characterized by left ventricular dysfunction or elevated intracardiac pressures. Research supports that microRNAs (miRs) participate in HF by regulating targeted genes. Hence, the current study set out to study the role of HDAC3-medaited miR-18a in HF by targeting ADRB3.
methodsFirstly, HF mouse models were established by ligation of the left coronary artery at the lower edge of the left atrial appendage, and HF cell models were generated in the cardiomyocytes, followed by ectopic expression and silencing experiments. Numerous parameters including left ventricular posterior wall dimension (LVPWD), interventricular septal dimension (IVSD), left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LEVDP), heart rate (HR), left ventricular pressure rise rate (+ dp/dt) and left ventricular pressure drop rate (-dp/dt) were measured in the mice. In addition, apoptosis in the mice was detected by means of TUNEL staining, while RT-qPCR and Western blot analysis were performed to detect miR-18a, HDAC3, ADRB3, cMyb, MMP-9, Collagen 1 and TGF-β1 expression patterns. Dual luciferase reporter assay validated the targeting relationship between ADRB3 and miR-18a. Cardiomyocyte apoptosis was determined by means of flow cytometry.
resultsHDAC3 and ADRB3 were up-regulated and miR-18a was down-regulated in HF mice and cardiomyocytes. In addition, HDAC3 could reduce the miR-18a expression, and ADRB3 was negatively-targeted by miR-18a. After down-regulation of HDAC3 or ADRB3 or over-expression of miR-18a, IVSD, LVEDD, LVESD and LEVDP were found to be decreased but LVPWD, LVEF, LVFS, LVSP, + dp/dt, and -dp/dt were all increased in the HF mice, whereas fibrosis, hypertrophy and apoptosis of HF cardiomyocytes were declined.
conclusionCollectively, our findings indicate that HDAC3 silencing confers protection against HF by inhibiting miR-18a-targeted ADRB3.
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