Epigenetic Regulation and Molecular Mechanisms in Cardiovascular Diseases: A Review of Recent Advances and Therapeutic Implications

TL;DR

This review explores how epigenetic changes contribute to heart diseases and highlights new therapies targeting these mechanisms.

Contribution

The paper synthesizes recent advances in epigenetic regulation and its therapeutic potential in cardiovascular diseases.

Findings

DNA methylation, histone modifications, and non-coding RNAs regulate gene expression in cardiovascular diseases.

Epigenetic alterations interact with inflammation and oxidative stress pathways to cause vascular dysfunction.

Therapies targeting epigenetic mechanisms show cardioprotective effects in experimental and clinical studies.

Abstract

Cardiovascular diseases (CVDs) remain the leading cause of death worldwide, with growing evidence indicating that epigenetic mechanisms play a central role in their onset and progression. This review provides a comprehensive overview of current knowledge on the epigenetic regulation and molecular mechanisms involved in CVDs, as well as their potential therapeutic implications. The findings demonstrate that DNA methylation, histone modifications, and non-coding RNAs are key regulators of gene expression associated with cardiac hypertrophy, atherosclerosis, myocardial infarction, and heart failure. Interactions between epigenetic alterations and inflammatory or oxidative stress pathways further contribute to endothelial dysfunction and vascular remodeling. Emerging therapeutic strategies targeting these mechanisms, including histone deacetylase inhibitors, DNA methyltransferase inhibitors, and RNA-based therapeutics, show promising cardioprotective effects in experimental and early clinical studies. Overall, this review underscores the significance of epigenetic regulation in cardiovascular pathophysiology and highlights the potential of epigenetic-based interventions as a foundation for precision medicine and novel therapeutic approaches in cardiology.

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