ArticleThe Journal of nutritional biochemistry2020
Emodin and emodin-rich rhubarb inhibits histone deacetylase (HDAC) activity and cardiac myocyte hypertrophy.
Article in The Journal of nutritional biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 45 citations in OpenAlex.
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- From Gut to Heart: Targeting Trimethylamine N-Oxide as a Novel Strategy in Heart Failure Management.Biomolecules · 2025Review
- Recent Insights into the Creation of Histone Deacetylase Inhibitors for the Treatment of Human Diseases.International journal of molecular sciences · 2025Review
- Exploring the Therapeutic Potential of Natural Compounds and Plant Extracts in Human Health.Biomolecules · 2025Article
- Emodin mitigates rheumatoid arthritis through direct binding to TNF-α.Frontiers in pharmacology · 2025Article
- Chromatin modifiers in human disease: from functional roles to regulatory mechanisms.Molecular biomedicine · 2024Review
- Recent advances of traditional Chinese medicine against cardiovascular disease: overview and potential mechanisms.Frontiers in endocrinology · 2024Review
- Emodin Inhibited Pathological Cardiac Hypertrophy in Response to Angiotensin-Induced Hypertension and Altered the Gut Microbiome.Biomolecules · 2023Article
- Review
- Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials.Signal transduction and targeted therapy · 2022Review
- Emodin in cardiovascular disease: The role and therapeutic potential.Frontiers in pharmacology · 2022Review
- IFN-γ and LPS Induce Synergistic Expression of CCL2 in Monocytic Cells via H3K27 Acetylation.Journal of inflammation research · 2022Article
- Activators of alpha synuclein expression identified by reporter cell line-based high throughput drug screen.Scientific reports · 2021Article
- Cardiac Energy Metabolism in Heart Failure.Circulation research · 2021Review
- Divergent and Overlapping Roles for Selected Phytochemicals in the Regulation of Pathological Cardiac Hypertrophy.Molecules (Basel, Switzerland) · 2021Article
- Comprehensive Analysis of Pertinent Genes and Pathways in Atrial Fibrillation.Computational and mathematical methods in medicine · 2021Article
- Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug.Frontiers in pharmacology · 2020Review
- Emodin-induced cell cycle arrest: A promising approach for cancer therapy (Review).Medicine internationalReview
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Authors and funding
9 authors at 1 institution in 1 country.
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Abstract
Pathological cardiac hypertrophy is a classical hallmark of heart failure. At the molecular level, inhibition of histone deacetylase (HDAC) enzymes attenuate pathological cardiac hypertrophy in vitro and in vivo. Emodin is an anthraquinone that has been implicated in cardiac protection. However, it is not known if the cardio-protective actions for emodin are mediated through HDAC-dependent regulation of gene expression. Therefore, we hypothesized that emodin would attenuate pathological cardiac hypertrophy via inhibition of HDACs, and that these actions would be reflected in an emodin-rich food like rhubarb. In this study, we demonstrate that emodin and Turkish rhubarb containing emodin inhibit HDAC activity in vitro, with fast-on, slow-off kinetics. Moreover, we show that emodin increased histone acetylation in cardiomyocytes concomitant to global changes in gene expression; gene expression changes were similar to the well-established pan-HDAC inhibitor trichostatin A (TSA). We additionally present evidence that emodin inhibited phenylephrine (PE) and phorbol myristate acetate (PMA)-induced hypertrophy in neonatal rat ventricular myocytes (NRVMs). Lastly, we demonstrate that the cardioprotective actions of emodin are translated to an angiotensin II (Ang) mouse model of cardiac hypertrophy and fibrosis and are linked to HDAC inhibition. These data suggest that emodin blocked pathological cardiac hypertrophy, in part, by inhibiting HDAC-dependent gene expression changes.
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