KLOTHO methylation is linked to uremic toxins and chronic kidney disease
Journal
Kidney International
Journal Volume
81
Journal Issue
7
Pages
611-612
Date Issued
2012
Author(s)
Young G.-H.
Abstract
Epigenetic regulation plays a major role in uremic toxin-induced chronic kidney disease (CKD) progression. The KLOTHO protein is a key modulator of homeostasis in renal function. Uremic toxin accumulation can induce DNA methyltransferase (DNMT) protein expression, which is involved in the silencing of KLOTHO through hypermethylation. Treatment with DNMT inhibitors can induce a hypermethylated status of KLOTHO and suppress mRNA and protein expression. Epigenetic targeting of specific genes may become an effective strategy to prevent progression of uremia-related CKD. ? 2012 International Society of Nephrology.
SDGs
Other Subjects
DNA methyltransferase; fibroblast growth factor 23; indican; Klotho protein; messenger RNA; reactive oxygen metabolite; somatomedin C; uremic toxin; bioaccumulation; chronic kidney disease; disease association; DNA methylation; DNA modification; down regulation; epigenetics; gene overexpression; gene silencing; genetic association; human; inflammation; kidney dysfunction; nonhuman; oxidative stress; pathogenesis; priority journal; protein expression; protein function; protein methylation; review; signal transduction; uremia
Publisher
Nature Publishing Group
Type
note