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Editorial
. 2018 Nov;72(5):1084-1086.
doi: 10.1161/HYPERTENSIONAHA.118.11755.

De Novo DNA (de)Methylation in the Kidney

Jia L Zhuo  1 , Xiao C Li  1
Affiliations
Editorial

De Novo DNA (de)Methylation in the Kidney

Jia L Zhuo et al. Hypertension. 2018 Nov.
No abstract available

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Figures

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A schematic hypothesis for the pathophysiological role of de novo DNA methylation (or demethylation) in the development of salt-sensitive hypertension. In salt-sensitive hypertension rats, treatment with a 4% or 8% high salt diet induces the DNA methylation (or demethylation) of the candidate genes for salt-sensitive hypertension and genes encoding neural peptides, adrenal hormones, and vasoactive peptides through the actions of DNA methyltransferase 3 (Dnmt3) and ten-eleven translocases (Tet). DNA methylation (or demethylation) is expected to alter the expression and activities of these genes and vasoactive peptides and their downstream signal transduction, which leads to the development of salt-sensitive hypertension. Conversely, molecular or pharmacological inhibition of Dnmt3a/Tet3 with anti-Dnmt3a/Tet3 GapmeRs may theoretically prevent the changes in the DNA methylation profiles of these candidate genes or vasoactive peptides. This in turn blocks the up- or downregulation of their gene expression, biological activities, and downstream signaling pathways, and attenuates salt-sensitive hypertension and target tissue injury.
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