A molecular target of vascular calcification in chronic kidney disease

Vascular calcification (VC) causes cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD), particularly those with end-stage kidney disease (ESKD) on maintenance dialysis treatment. Although many mechanisms have been proposed, their detailed effects remain incompletely...

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Main Author: Mohamed G. Atta
Format: Article
Language:English
Published: American Society for Clinical Investigation 2022-01-01
Series:The Journal of Clinical Investigation
Online Access:https://doi.org/10.1172/JCI156257
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author Mohamed G. Atta
author_facet Mohamed G. Atta
author_sort Mohamed G. Atta
collection DOAJ
description Vascular calcification (VC) causes cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD), particularly those with end-stage kidney disease (ESKD) on maintenance dialysis treatment. Although many mechanisms have been proposed, their detailed effects remain incompletely understood. In this issue of the JCI, Li et al. examined the molecular mechanism of the protective role of SIRT6 in VC in patients with CKD. Using in vitro and animal models of CKD, the authors demonstrated that SIRT6 prevents VC by suppressing the osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs). Mechanistically, SIRT6 bound and deacetylated the runt-related transcription factor 2 (Runx2), a key transcription factor for osteogenic differentiation, promoting its nuclear export for proteasome degradation. These studies provide a pathway in the pathogenesis of VC and justify investigating SIRT6 as a potential target in CKD.
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spelling doaj.art-f20e965078c2485d96be121145fcfe102022-12-22T03:37:05ZengAmerican Society for Clinical InvestigationThe Journal of Clinical Investigation1558-82382022-01-011321A molecular target of vascular calcification in chronic kidney diseaseMohamed G. AttaVascular calcification (VC) causes cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD), particularly those with end-stage kidney disease (ESKD) on maintenance dialysis treatment. Although many mechanisms have been proposed, their detailed effects remain incompletely understood. In this issue of the JCI, Li et al. examined the molecular mechanism of the protective role of SIRT6 in VC in patients with CKD. Using in vitro and animal models of CKD, the authors demonstrated that SIRT6 prevents VC by suppressing the osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs). Mechanistically, SIRT6 bound and deacetylated the runt-related transcription factor 2 (Runx2), a key transcription factor for osteogenic differentiation, promoting its nuclear export for proteasome degradation. These studies provide a pathway in the pathogenesis of VC and justify investigating SIRT6 as a potential target in CKD.https://doi.org/10.1172/JCI156257
spellingShingle Mohamed G. Atta
A molecular target of vascular calcification in chronic kidney disease
The Journal of Clinical Investigation
title A molecular target of vascular calcification in chronic kidney disease
title_full A molecular target of vascular calcification in chronic kidney disease
title_fullStr A molecular target of vascular calcification in chronic kidney disease
title_full_unstemmed A molecular target of vascular calcification in chronic kidney disease
title_short A molecular target of vascular calcification in chronic kidney disease
title_sort molecular target of vascular calcification in chronic kidney disease
url https://doi.org/10.1172/JCI156257
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