ArticleScientific reports2017
The histone 3 lysine 9 methyltransferase inhibitor chaetocin improves prognosis in a rat model of high salt diet-induced heart failure.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Regulation of mitochondrial biogenesis and energy metabolism in the heart.Chinese medical journal · 2026Review
- Article
- Methylation-centric epigenetic regulation in dilated cardiomyopathy: mechanisms, metabolic interplay, and translational potential.Frontiers in cardiovascular medicine · 2026Review
- The Role of Histone Methylation in Heart Failure: Epigenetic Mechanisms and Therapeutic Perspectives.Drug design, development and therapy · 2026Review
- Targeting KDM4C Prevents Heart Failure after Acute Myocardial Infarction Via Activation of SOS2.Journal of cardiovascular translational research · 2025Article
- Emerging Epigenetic Therapies for the Treatment of Cardiac Fibrosis.Biomedicines · 2025Review
- Epigenetics in Heart Failure.International journal of molecular sciences · 2024Review
- Epigenetic regulation of cardiovascular diseases induced by behavioral and environmental risk factors: Mechanistic, diagnostic, and therapeutic insights.FASEB bioAdvances · 2024Review
- Epigenetic regulation of sex dimorphism in cardiovascular health.Canadian journal of physiology and pharmacology · 2024Review
- Review
- An Updated Review on the Significance of DNA and Protein Methyltransferases and De-methylases in Human Diseases: From Molecular Mechanism to Novel Therapeutic Approaches.Current medicinal chemistry · 2024Review
- Chaetocin disrupts the SUV39H1-HP1 interaction independent of SUV39H1 methyltransferase activity.The Biochemical journal · 2023Article
- Emerging epigenetic therapies of cardiac fibrosis and remodelling in heart failure: from basic mechanisms to early clinical development.Cardiovascular research · 2023Review
- Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials.Signal transduction and targeted therapy · 2022Review
- Whole blood transcriptomic profiling identifies molecular pathways related to cardiovascular mortality in heart failure.European journal of heart failure · 2022Article
- G9α-dependent histone H3K9me3 hypomethylation promotes overexpression of cardiomyogenesis-related genes in foetal mice.Journal of cellular and molecular medicine · 2020Article
- Multiple Levels of PGC-1α Dysregulation in Heart Failure.Frontiers in cardiovascular medicine · 2020Review
- Moderate Exercise in Spontaneously Hypertensive Rats Is Unable to Activate the Expression of Genes Linked to Mitochondrial Dynamics and Biogenesis in Cardiomyocytes.Frontiers in endocrinology · 2020Article
- The Mitochondrial Unfolded Protein Response: A Hinge Between Healthy and Pathological Aging.Frontiers in aging neuroscience · 2020Review
- Double the Chemistry, Double the Fun: Structural Diversity and Biological Activity of Marine-Derived Diketopiperazine Dimers.Marine drugs · 2019Review
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone acetylation has been linked to cardiac hypertrophy and heart failure. However, the pathological implications of changes in histone methylation and the effects of interventions with histone methyltransferase inhibitors for heart failure have not been fully clarified. Here, we focused on H3K9me3 status in the heart and investigated the effects of the histone H3K9 methyltransferase inhibitor chaetocin on prognoses in Dahl salt-sensitive rats, an animal model of chronic heart failure. Chaetocin prolonged survival and restored mitochondrial dysfunction. ChIP-seq analysis demonstrated that chronic stress to the heart induced H3K9me3 elevation in thousands of repetitive elements, including intronic regions of mitochondria-related genes, such as the gene encoding peroxisome proliferator-activated receptor-gamma coactivator 1 alpha. Furthermore, chaetocin reversed this effect on these repetitive loci. These data suggested that excessive heterochromatinization of repetitive elements of mitochondrial genes in the failing heart may lead to the silencing of genes and impair heart function. Thus, chaetocin may be a potential therapeutic agent for chronic heart failure.
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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.