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Purpose <p>Cardiovascular diseases (CVDs) continue to be the leading cause of death globally, driven by a complex interplay of genetic, epigenetic, and environmental factors. Traditional risk factors alone fail to explain the individual variability in disease susceptibility and progression. Recent advances in genomics and epigenomics have revealed key molecular mechanisms that regulate cardiovascular function, highlighting the importance of gene network dynamics and epigenetic regulation.</p> Methods <p>This review systematically analyzes peer-reviewed literature from the past decade sourced from electronic databases including PubMed and Google Scholar. It compiles the multifaceted roles of DNA methylation, histone modifications, chromatin remodeling, and noncoding RNAs in regulating cardiovascular gene expression, cellular phenotypes, and disease pathogenesis.</p> Results <p>DNA methylation influences the transcriptional activity of gene expression associated with atherosclerosis, myocardial infarction, and hypertension, while histone modifications and ATP-dependent chromatin remodeling regulate cardiac hypertrophy, fibrosis, and regeneration. Noncoding RNAs further&#xa0;act as critical regulators of angiogenesis, inflammation, and myocardial remodeling. Therapeutically, these findings have facilitated the development of epigenetic drugs and gene-editing technologies targeting specific molecular pathways involved in CVD progression. Emerging technologies such as CRISPR/Cas9, RNA-based therapies, and small-molecule inhibitors of epigenetic enzymes hold potential for correct abnormal gene expression patterns. Moreover, integrative multi-omics and systems biology&#xa0;approaches are advancing personalized treatment strategies, improving the accuracy and effectiveness of cardiovascular interventions.</p> Conclusion <p>Collectively, unraveling the complex molecular interactions among gene networks, epigenetic alterations, and targeted therapeutic mapping aims to combat CVD with better precision and efficacy.</p> Graphical Abstract <p></p>

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Molecular Interplay of Gene Network Dynamics, Epigenetic Regulation, and Therapeutic Mapping in Cardiovascular Disease

  • 期刊论文

  • 发表日期：

    2025年6月20日

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  • Md Rashedunnabi Akanda,
  • Md Shiblee Sadik Sabuj,
  • S. M. Abdus Salam,
  • Eshrat Jahan

摘要

Purpose

Cardiovascular diseases (CVDs) continue to be the leading cause of death globally, driven by a complex interplay of genetic, epigenetic, and environmental factors. Traditional risk factors alone fail to explain the individual variability in disease susceptibility and progression. Recent advances in genomics and epigenomics have revealed key molecular mechanisms that regulate cardiovascular function, highlighting the importance of gene network dynamics and epigenetic regulation.

Methods

This review systematically analyzes peer-reviewed literature from the past decade sourced from electronic databases including PubMed and Google Scholar. It compiles the multifaceted roles of DNA methylation, histone modifications, chromatin remodeling, and noncoding RNAs in regulating cardiovascular gene expression, cellular phenotypes, and disease pathogenesis.

Results

DNA methylation influences the transcriptional activity of gene expression associated with atherosclerosis, myocardial infarction, and hypertension, while histone modifications and ATP-dependent chromatin remodeling regulate cardiac hypertrophy, fibrosis, and regeneration. Noncoding RNAs further act as critical regulators of angiogenesis, inflammation, and myocardial remodeling. Therapeutically, these findings have facilitated the development of epigenetic drugs and gene-editing technologies targeting specific molecular pathways involved in CVD progression. Emerging technologies such as CRISPR/Cas9, RNA-based therapies, and small-molecule inhibitors of epigenetic enzymes hold potential for correct abnormal gene expression patterns. Moreover, integrative multi-omics and systems biology approaches are advancing personalized treatment strategies, improving the accuracy and effectiveness of cardiovascular interventions.

Conclusion

Collectively, unraveling the complex molecular interactions among gene networks, epigenetic alterations, and targeted therapeutic mapping aims to combat CVD with better precision and efficacy.

Graphical Abstract