Epigenetic contributions to hypertension

This 2016 Australian review subject was epigenetic contributions to hypertension:

“Hypertension (HT) affects more than 1 billion people globally and is a major risk factor for stroke, chronic kidney disease, and myocardial infarction.

Essential hypertension (EH) is a complex, polygenic condition with no single causative agent. There is increasing evidence that epigenetic modifications are as important as genetic predisposition in the development of EH.

Many epigenetic studies are, however, limited by the fact that only blood is studied rather than the effector tissues. The utility of blood methylation status in epigenetic research is yet to be determined. Furthermore, the polygenic complexity of HT and the limited knowledge on some of the non-coding RNAs makes it more challenging to decipher the exact mechanisms involved.”

The review had sections for hypertension studies on DNA methylation, histone modification, and microRNA/other non-coding RNA types. Here’s a sample of the findings:

“HSD11B2-mediated degradation of cortisol to cortisone is disrupted when the promoter region of the HSD11B2 gene is hypermethylated. The resulting imbalance in the active metabolites of cortisol and cortisone, tetrahydrocortisol, and tetrahydocortisone, respectively, promotes the onset of HT.

Histone modification affecting arterial pressure levels has been documented in a variety of human and animal tissues, including vascular smooth muscle. Vascular oxidative stress can contribute to endothelial dysfunction—a hallmark of HT—and the development of HT.

Two miRNAs (has-miR-181a and has-miR-663) with the ability to bind to the 3′ UTR of renin mRNA were found to be under-expressed in EH. These miRNAs were able to regulate the expression of a reporter gene and renin-mRNA itself, which explains over-expression of renin mRNA seen in EH kidney.”

The publisher, International Journal of Molecular Sciences, makes ALL of its articles open access. Another of its requirements is: