ArticleLaboratory investigation; a journal of technical methods and pathology2020
Myocardial tissue-specific Dnmt1 knockout in rats protects against pathological injury induced by Adriamycin.
Article in Laboratory investigation; a journal of technical methods and pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- Nutritional Prevention of Oxidative Stress-Induced Cardiotoxicity in Pediatric Cardio-Oncology: Molecular Mechanisms and Translational Perspectives-A Narrative Review.International journal of molecular sciences · 2026Review
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- Nuclear Proteome Map of Mouse Heart Chambers.Molecular & cellular proteomics : MCP · 2026Article
- Interconnected Pathways and Therapeutic Implications for Cardiovascular Aging and Diseases.JACC. Asia · 2026Review
- Research progress on programmed cell death of cardiomyocytes in pressure-overload hypertrophic cardiomyopathy.Apoptosis : an international journal on programmed cell death · 2025Review
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Cytochrome P450 2E1 aggravates DXR-induced myocardial injury through imbalanced mitochondrial OPA1.Cell communication and signaling : CCS · 2025Article
- The role and mechanism of epigenetics in anticancer drug-induced cardiotoxicity.Basic research in cardiology · 2025Review
- Methylations in dilated cardiomyopathy and heart failure.Frontiers in cardiovascular medicine · 2025Review
- Non-coding RNAs in heart failure: epigenetic regulatory mechanisms and therapeutic potential.Frontiers in genetics · 2025Review
- Epigenetic Study of Cohort of Monozygotic Twins With Hypertrophic Cardiomyopathy Due to MYBPC3 (Cardiac Myosin-Binding Protein C).Journal of the American Heart Association · 2024Article
- Epigenetic regulation of sex dimorphism in cardiovascular health.Canadian journal of physiology and pharmacology · 2024Review
- Reduced DNMT1 levels induce cell apoptosis via upregulation of METTL3 in cardiac hypertrophy.Heliyon · 2024Article
- Application and perspective of CRISPR/Cas9 genome editing technology in human diseases modeling and gene therapy.Frontiers in genetics · 2024Review
- Unveiling shared biomarkers and therapeutic targets between systemic lupus erythematosus and heart failure through bioinformatics analysis.Frontiers in medicine · 2024Article
- Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023Review
- Review
- Bioactive Compounds and Cardiac Fibrosis: Current Insight and Future Prospect.Journal of cardiovascular development and disease · 2023Review
- Integration of epigenetic regulatory mechanisms in heart failure.Basic research in cardiology · 2023Review
- Cardiac-specific Trim44 knockout in rat attenuates isoproterenol-induced cardiac remodeling via inhibition of AKT/mTOR pathway.Disease models & mechanisms · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Novel molecular mechanisms of the pathophysiology of heart failure (HF) are continuously being discovered, including epigenetic regulation. Among epigenetic marks, the role of DNA hypomethylation in shaping heart morphology and function in vivo and the pathogenesis of cardiomyopathy and/or HF, especially in adults, has not been clearly established. Here we show that the strong expression of DNA methyltransferase 1 (Dnmt1) is obviously downregulated in the WT adult rat heart with age. By contrast, the expression of Dnmt1 is upregulated suddenly in heart tissues from pressure overload-induced HF mice and adriamycin-induced cardiac injury and HF mice, consistent with the increased expression of Dnmt1 observed in familial hypertrophic cardiomyopathy (FHCM) patients. To further assess the role of Dnmt1, we generated myocardium-specific Dnmt1 knockout (Dnmt1 KO) rats using CRISPR-Cas9 technology. Echocardiographic and histopathological examinations demonstrated that Dnmt1 deficiency is associated with resistance to cardiac pathological changes and protection at the global and organization levels in response to pathological stress. Furthermore, Dnmt1 deficiency in the myocardium restricts the expressional reprogramming of genes and activates pathways involved in myocardial protection and anti-apoptosis in response to pathological stress. Transcriptome and genome-wide DNA methylation analyses revealed that these changes in regulation are linked to alterations in the methylation status of genes due to Dnmt1 knockout. The present study is the first to investigate in vivo the impact of genome-wide cardiac DNA methyltransferase deficiency on physiological development and the pathological processes of heart tissues in response to stress. The exploration of the role of epigenetics in the development, modification, and prevention of cardiomyopathy and HF is in a very preliminary stage but has an infinite future.
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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.