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Epigenetic regulation in hypertension: mechanistic insights and environmental influences
Sravan Perla1,2, Alladi Charanraj Goud3, Matthew Liu4
1Department of Pathology, Microbiology and Immunology, New York Medical College, Valhalla, NY, United States.
Insights
Epigenetic changes, driven by high-salt diets, can alter gene expression related to blood pressure regulation. These persistent epigenetic modifications contribute to salt-sensitive hypertension and offer potential therapeutic targets.
Area of Science:
- Cardiovascular Science
- Epigenetics
- Hypertension Research
Background:
- Hypertension is a major global health issue linked to cardiovascular, renal, and cerebrovascular diseases.
- Epigenetic regulation, including DNA methylation, histone modifications, and non-coding RNAs, plays a crucial role in blood pressure control and vascular pathology.
- Aberrant epigenetic signatures in key tissues affect pathways regulating vascular tone, sodium handling, oxidative stress, and inflammation.
Purpose of the Study:
- To explore the role of epigenetic mechanisms in blood pressure regulation and vascular pathology.
- To investigate how environmental factors, particularly high-salt diet, influence the epigenetic landscape of genes involved in blood pressure control.
- To identify potential therapeutic strategies targeting epigenetic modifications for hypertension treatment.
Main Methods:
- Review of accumulating evidence on epigenetic mechanisms (DNA methylation, histone modifications, non-coding RNAs) in blood pressure regulation.
- Analysis of studies examining the impact of high-salt diet on epigenetic signatures in relevant tissues.
- Examination of epigenetic alterations in renin-angiotensin-aldosterone system (RAAS) genes (AGT, REN, ACE, AT1R).
Main Results:
- Epigenetic modifications in RAAS genes contribute to sustained activation of vasoconstrictive and sodium-retentive signaling.
- Chronic high-salt diet exposure alters DNA methylation, histone acetylation, and microRNA profiles, enhancing RAAS activity and vascular dysfunction.
- High-salt diet-induced epigenetic changes can persist, creating an 'epigenetic memory' contributing to salt-sensitive hypertension.
Conclusions:
- Epigenetic reprogramming of RAAS-related gene networks by environmental factors provides insight into hypertension's molecular basis.
- Understanding these epigenetic mechanisms opens new therapeutic avenues for hypertension.
- Potential therapies include DNA methyltransferase inhibitors, histone deacetylase inhibitors, and RNA-based precision therapies to reverse maladaptive epigenetic imprints.
Abstract:
Hypertension is a leading global cause of cardiovascular, renal, and cerebrovascular morbidity. Beyond classical genetic and environmental determinants, accumulating evidence highlights epigenetic regulation as a key contributor to blood pressure control and vascular pathology. Epigenetic mechanisms, including DNA methylation, histone post-translational modifications, and non-coding RNAs, govern gene expression without altering the underlying DNA sequence, thereby linking environmental and physiological stimuli to stable transcriptional changes. Aberrant epigenetic signatures have been identified in vascular, renal, and endocrine tissues integral to blood pressure regulation, influencing pathways that mediate vascular tone, sodium handling, oxidative stress, and inflammation. Among these, differential methylation and histone modification of renin-angiotensin-aldosterone system (RAAS) genes, including AGT, REN, ACE, and AT1R, have been shown to promote sustained activation of vasoconstrictive and sodium-retentive signaling cascades. Chronic exposure to a high-salt diet (HSD) represents a potent environmental modifier of this epigenetic landscape. Excess dietary sodium can alter CpG methylation patterns, histone acetylation states, and microRNA profiles across multiple tissues, leading to enhanced RAAS activity and vascular dysfunction. These HSD-induced alterations often persist despite subsequent sodium normalization, reflecting an enduring "epigenetic memory" of dietary stress that contributes to salt-sensitive hypertension. Understanding how HSD and other environmental factors reprogram RAAS-related gene networks through epigenetic mechanisms provides critical insight into the molecular basis of hypertension. Moreover, these findings open new avenues for therapeutic intervention utilizing DNA methyltransferase and histone deacetylase inhibitors, as well as RNA-based precision therapies aimed at reversing the maladaptive epigenetic imprint underlying chronic blood pressure elevation.
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