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Endothelial Dysfunction in Patients with Chronic Kidney Disease Results from Advanced Glycation End Products (AGE)-Mediated Inhibition of Endothelial Nitric Oxide Synthase through RAGE Activation
Author(s) -
Ellena A. Linden,
Weijing Cai,
John Cijiang He,
Xue Chen,
Li Zhu,
Jonathan Winston,
Helen Vlassara,
Jaime Uribarri
Publication year - 2008
Publication title -
clinical journal of the american society of nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.755
H-Index - 151
eISSN - 1555-905X
pISSN - 1555-9041
DOI - 10.2215/cjn.04291007
Subject(s) - glycation , advanced glycation end product , endothelial dysfunction , medicine , reactive hyperemia , kidney disease , endocrinology , nitric oxide synthase , endothelium , diabetes mellitus , nitric oxide , vasodilation
Advanced glycation end products, known pro-inflammatory and pro-oxidative compounds that accumulate in patients with chronic kidney disease, may play a major role in their high prevalence of endothelial dysfunction and subsequent cardiovascular disease. This study examined the association of advanced glycation end product accumulation with cellular receptor for advanced glycation end product expression and endothelial dysfunction as well as the mechanisms of this association in chronic kidney disease.

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