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Epigenetic-sensitive pathways in personalized therapy of major cardiovascular diseases
Concetta Schiano1, Giuditta Benincasa1, Monica Franzese2
1Clinical Department of Internal Medicine and Specialistics, Department of Advanced Clinical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy.
Abstract:
The complex pathobiology underlying cardiovascular diseases (CVDs) has yet to be explained. Aberrant epigenetic changes may result from alterations in enzymatic activities, which are responsible for putting in and/or out the covalent groups, altering the epigenome and then modulating gene expression. The identification of novel individual epigenetic-sensitive trajectories at single cell level might provide additional opportunities to establish predictive, diagnostic and prognostic biomarkers as well as drug targets in CVDs. To date, most of studies investigated DNA methylation mechanism and miRNA regulation as epigenetics marks. During atherogenesis, big epigenetic changes in DNA methylation and different ncRNAs, such as miR-93, miR-340, miR-433, miR-765, CHROME, were identified into endothelial cells, smooth muscle cells, and macrophages. During man development, lipid metabolism, inflammation and homocysteine homeostasis, alter vascular transcriptional mechanism of fundamental genes such as ABCA1, SREBP2, NOS, HIF1. At histone level, increased HDAC9 was associated with matrix metalloproteinase 1 (MMP1) and MMP2 expression in pro-inflammatory macrophages of human carotid plaque other than to have a positive effect on toll like receptor signaling and innate immunity. HDAC9 deficiency promoted inflammation resolution and reverse cholesterol transport, which might block atherosclerosis progression and promote lesion regression. Here, we describe main human epigenetic mechanisms involved in atherosclerosis, coronary heart disease, ischemic stroke, peripheral artery disease; cardiomyopathy and heart failure. Different epigenetics mechanisms are activated, such as regulation by circular RNAs, as MICRA, and epitranscriptomics at RNA level. Moreover, in order to open new frontiers for precision medicine and personalized therapy, we offer a panoramic view on the most innovative bioinformatic tools designed to identify putative genes and molecular networks underlying CVDs in man.
Insights
Epigenetic changes significantly impact cardiovascular diseases (CVDs). Understanding these epigenetic mechanisms offers new avenues for developing predictive biomarkers and targeted therapies for conditions like atherosclerosis and heart failure.
Area of Science:
- Cardiovascular Epigenetics
- Molecular Medicine
- Biomarker Discovery
Background:
- Cardiovascular diseases (CVDs) exhibit complex pathobiology not fully explained by current models.
- Aberrant epigenetic modifications, involving enzymatic alterations to the epigenome, are increasingly recognized as key players in CVD development.
- Single-cell level identification of epigenetic-sensitive trajectories is crucial for advancing predictive, diagnostic, and prognostic strategies in CVD.
Purpose of the Study:
- To elucidate the primary human epigenetic mechanisms implicated in major cardiovascular diseases.
- To explore novel epigenetic regulators, including non-coding RNAs and epitranscriptomic modifications.
- To provide an overview of bioinformatic tools for identifying molecular networks in CVDs for precision medicine.
Main Methods:
- Review of existing literature on epigenetic mechanisms in atherosclerosis, coronary heart disease, ischemic stroke, peripheral artery disease, cardiomyopathy, and heart failure.
- Analysis of DNA methylation, microRNA (miRNA) regulation, and histone modifications (e.g., HDAC9).
- Investigation of circular RNAs (circRNAs) and epitranscriptomics.
Main Results:
- Epigenetic alterations, including DNA methylation and specific miRNAs (e.g., miR-93, miR-340), are identified in endothelial cells, smooth muscle cells, and macrophages during atherogenesis.
- Histone deacetylase 9 (HDAC9) is linked to matrix metalloproteinase expression and inflammation in human carotid plaques; its deficiency may resolve inflammation and reverse cholesterol transport.
- Emerging mechanisms like circular RNAs (e.g., MICRA) and epitranscriptomics are involved in CVD pathogenesis.
Conclusions:
- Epigenetic dysregulation is a fundamental aspect of cardiovascular disease pathology.
- Targeting epigenetic modifications presents a promising strategy for developing novel therapeutic interventions and personalized medicine approaches for CVDs.
- Advanced bioinformatic tools are essential for dissecting complex molecular networks and identifying therapeutic targets in cardiovascular medicine.
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