ArticleJournal of cellular and molecular medicine2019
Anacardic acid attenuates pressure-overload cardiac hypertrophy through inhibiting histone acetylases.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 46 citations in OpenAlex.
- Exercise ModulatesInternational journal of molecular sciences · 2026Article
- Mitigation of Injury from Myocardial Infarction by Pentamidine, an Inhibitor of the Acetyltransferase Tip60.Cardiovascular drugs and therapy · 2026Article
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- Gene expression profiles, potential targets and treatments of cardiac remodeling.Molecular and cellular biochemistry · 2025Review
- Role and Mechanism of Lamellar Derived Growth Factor /AKT Pathway in Ventricular Remodeling Induced by Pressure Overload.Cell biochemistry and biophysics · 2025Article
- Acetylation in Cardiac Aging: Molecular Mechanism and Therapeutic Approaches.Results and problems in cell differentiation · 2025Review
- Cfp1 Controls Cardiomyocyte Maturation by Modifying Histone H3K4me3 of Structural, Metabolic, and Contractile Related Genes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Anserine, a Histidine-Containing Dipeptide, Suppresses Pressure Overload-Induced Systolic Dysfunction by Inhibiting Histone Acetyltransferase Activity of p300 in Mice.International journal of molecular sciences · 2024Article
- The efficacy of botanical drugs in orchestrating epigenetic modifications for ameliorating metabolic disorders.Frontiers in pharmacology · 2024Article
- Macrophage LMO7 deficiency facilitates inflammatory injuryActa pharmaceutica Sinica. B · 2023Article
- SIRT6 mediated histone H3K9ac deacetylation involves myocardial remodelling through regulating myocardial energy metabolism in TAC mice.Journal of cellular and molecular medicine · 2023Article
- Decreased HAT1 expression in granulosa cells disturbs oocyte meiosis during mouse ovarian aging.Reproductive biology and endocrinology : RB&E · 2023Article
- Pharmacological inhibition of the acetyltransferase Tip60 mitigates myocardial infarction injury.Disease models & mechanisms · 2023Article
- Roles of histone acetylation sites in cardiac hypertrophy and heart failure.Frontiers in cardiovascular medicine · 2023Review
- EGCG prevents pressure overload‑induced myocardial remodeling by downregulating overexpression of HDAC5 in mice.International journal of molecular medicine · 2022Article
- Review
- Interactions between the ERK1/2 signaling pathway and PCAF play a key role in PE‑induced cardiomyocyte hypertrophy.Molecular medicine reports · 2021Article
- Histone Acetylation Domains Are Differentially Induced during Development of Heart Failure in Dahl Salt-Sensitive Rats.International journal of molecular sciences · 2021Article
- Steric-Free Bioorthogonal Labeling of Acetylation Substrates Based on a Fluorine-Thiol Displacement Reaction.Journal of the American Chemical Society · 2021Article
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy has become a major cardiovascular problem wordwide and is considered the early stage of heart failure. Treatment and prevention strategies are needed due to the suboptimal efficacy of current treatment methods. Recently, many studies have demonstrated the important role of histone acetylation in myocardium remodelling along with cardiac hypertrophy. A Chinese herbal extract containing anacardic acid (AA) is known to possess strong histone acetylation inhibitory effects. In previous studies, we demonstrated that AA could reverse alcohol-induced cardiac hypertrophy in an animal model at the foetal stage. Here, we investigated whether AA could attenuate cardiac hypertrophy through the modulation of histone acetylation and explored its potential mechanisms in the hearts of transverse aortic constriction (TAC) mice. This study showed that AA attenuated hyperacetylation of acetylated lysine 9 on histone H3 (H3K9ac) by inhibiting the expression of p300 and p300/CBP-associated factor (PCAF) in TAC mice. Moreover, AA normalized the transcriptional activity of the heart nuclear transcription factor MEF2A. The high expression of cardiac hypertrophy-linked genes (ANP, β-MHC) was reversed through AA treatment in the hearts of TAC mice. Additionally, we found that AA improved cardiac function and survival rate in TAC mice. The current results further highlight the mechanism by which histone acetylation is controlled by AA treatment, which may help prevent and treat hypertrophic cardiomyopathy.
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