Histone Modifications and Their Contributions to Hypertension

Abstract

Essential hypertension, a multifaceted disorder, is a worldwide health problem. A complex network of genetic, epigenetic, physiological, and environmental components regulates blood pressure (BP), and any dysregulation of this network may result in hypertension. Growing evidence suggests a role for epigenetic factors in BP regulation. Any alterations in the expression or functions of these epigenetic regulators may dysregulate various determinants of BP, thereby promoting the development of hypertension. Histone posttranslational modifications are critical epigenetic regulators that have been implicated in hypertension. Several studies have demonstrated a clear association between the increased expression of some histone-modifying enzymes, especially HDACs (histone deacetylases), and hypertension. In addition, treatment with HDAC inhibitors lowers BP in hypertensive animal models, providing an excellent opportunity to design new drugs to treat hypertension. In this review, we discuss the potential contribution of different histone modifications to the regulation of BP.

Epigenetics of hypertension as a risk factor for the development of coronary artery disease in type 2 diabetes mellitus

“…Epigenetic modifications have also been implicated in the regulation of vascular function in hypertension ( 82 ). Changes in DNA methylation and histone modifications can alter the expression of genes involved in vascular smooth muscle contraction, endothelial function, and vascular remodeling, contributing to hypertension development ( 129 ). Future research should focus on elucidating the specific epigenetic changes associated with vascular function-dependent hypertension and developing targeted therapies to restore vascular function and reduce blood pressure.…”

Maternally Inherited Essential Hypertension May Be Associated with the Mutations in Mitochondrial tRNAGlu Gene

“…However, the homoplasmic form, late onset and incomplete penetrance of EH observed in these Chinese families carrying the tRNA Glu mutations suggested that the m.A14693G and m.A14696G mutations were involved in the development of EH but may be insufficient to produce a clinical phenotype; hence, other factors such as nuclear genes (ADD1; ALDH1A3), 49,50 environmental components (air pollution), epigenetic modification (histone modification, DNA methylation) 51,52 and personal lifestyle (smoking or high salt intake) may contribute to EH expression in these two families. 53,54 In particular, mito-nuclear communication played a putative role in the pathogenesis of cardiovascular disease.…”