Epigenetic Regulation of Cardiovascular Physiology: Role of DNA Methylation and Histone Modification in Heart Failure Pathogenesis and Therapy
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2026
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| author | Ramyashree Narayana*, Shivprasad Sanjay Dhage |
| author_facet | Ramyashree Narayana*, Shivprasad Sanjay Dhage |
| contents | <p><span>Heart failure (HF) stands as the culminating expression of virtually all serious cardiovascular disorders, burdening more than 64 million people worldwide and carrying five-year mortality figures that rival many solid-organ malignancies. Although haemodynamic overload and neurohormonal activation have historically framed our understanding of HF progression, a growing body of mechanistic work has identified epigenetic dysregulation — most notably aberrant DNA methylation and abnormal histone modification — as a primary driver of the transcriptional reprogramming that underlies myocardial hypertrophy, interstitial fibrosis, contractile impairment, and metabolic rigidity. Deciphering how reversible biochemical marks overlaid on the cardiac genome respond to pressure overload, ischaemic hypoxia, hormonal activation, and the cumulative effects of ageing is therefore not an academic exercise; it discloses a pharmacological target space wholly distinct from the receptor antagonists and enzyme blockers at the core of current guideline-directed therapy. This review integrates peer-reviewed evidence identified through systematic literature searches of MEDLINE, EMBASE, and Web of Science, employing search terms spanning DNA methylation, histone acetylation, histone deacetylase, H3K4me3, H3K27me3, cardiac hypertrophy, myocardial fibrosis, and heart failure, supplemented by manual screening of major cardiology and epigenetics journal archives from 2000 to 2024. Ninety primary and review sources were selected on the basis of methodological rigour, mechanistic insight, and translational relevance. Circulating methylation signatures and plasma HDAC activity indices offer diagnostic and prognostic resolution beyond established biomarkers. HDAC inhibitors, DNMT inhibitors, BET bromodomain inhibitors, and</span><span>EZH2 inhibitors have demonstrated cardiac benefit in preclinical systems, with selected agents progressing to early-phase clinical trials.Realising this potential demands more </span></p> <p><span> </span></p> |
| format | Recurso digital |
| id | zenodo_https___doi_org_10_5281_zenodo_19641350 |
| institution | Zenodo |
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| publishDate | 2026 |
| publisher | Zenodo |
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| spellingShingle | Epigenetic Regulation of Cardiovascular Physiology: Role of DNA Methylation and Histone Modification in Heart Failure Pathogenesis and Therapy Ramyashree Narayana*, Shivprasad Sanjay Dhage epigenetics; DNA methylation; histone modification; HDAC inhibitors; DNMT inhibitors; cardiac hypertrophy; myocardial fibrosis; heart failure; CpG islands; chromatin remodelling; non-coding RNA; epigenetic biomarkers; BET inhibitors; EZH2; cardiovascular physiology. <p><span>Heart failure (HF) stands as the culminating expression of virtually all serious cardiovascular disorders, burdening more than 64 million people worldwide and carrying five-year mortality figures that rival many solid-organ malignancies. Although haemodynamic overload and neurohormonal activation have historically framed our understanding of HF progression, a growing body of mechanistic work has identified epigenetic dysregulation — most notably aberrant DNA methylation and abnormal histone modification — as a primary driver of the transcriptional reprogramming that underlies myocardial hypertrophy, interstitial fibrosis, contractile impairment, and metabolic rigidity. Deciphering how reversible biochemical marks overlaid on the cardiac genome respond to pressure overload, ischaemic hypoxia, hormonal activation, and the cumulative effects of ageing is therefore not an academic exercise; it discloses a pharmacological target space wholly distinct from the receptor antagonists and enzyme blockers at the core of current guideline-directed therapy. This review integrates peer-reviewed evidence identified through systematic literature searches of MEDLINE, EMBASE, and Web of Science, employing search terms spanning DNA methylation, histone acetylation, histone deacetylase, H3K4me3, H3K27me3, cardiac hypertrophy, myocardial fibrosis, and heart failure, supplemented by manual screening of major cardiology and epigenetics journal archives from 2000 to 2024. Ninety primary and review sources were selected on the basis of methodological rigour, mechanistic insight, and translational relevance. Circulating methylation signatures and plasma HDAC activity indices offer diagnostic and prognostic resolution beyond established biomarkers. HDAC inhibitors, DNMT inhibitors, BET bromodomain inhibitors, and</span><span>EZH2 inhibitors have demonstrated cardiac benefit in preclinical systems, with selected agents progressing to early-phase clinical trials.Realising this potential demands more </span></p> <p><span> </span></p> |
| title | Epigenetic Regulation of Cardiovascular Physiology: Role of DNA Methylation and Histone Modification in Heart Failure Pathogenesis and Therapy |
| topic | epigenetics; DNA methylation; histone modification; HDAC inhibitors; DNMT inhibitors; cardiac hypertrophy; myocardial fibrosis; heart failure; CpG islands; chromatin remodelling; non-coding RNA; epigenetic biomarkers; BET inhibitors; EZH2; cardiovascular physiology. |
| url | https://doi.org/10.5281/zenodo.19641350 |