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Title: Uric acid as a mediator of endothelial dysfunction, inflammation, and vascular disease.
Austin Authors: Kanellis, John;Kang, Duk-Hee
Affiliation: Department of Nephrology and Medicine, University of Melbourne, Austin Hospital, Australia
Issue Date: 1-Jan-2005
Publication information: Seminars in Nephrology; 25(1): 39-42
Abstract: Recent experimental findings have led to renewed interest in the possible role of uric acid in the pathogenesis of both hypertension and vascular disease. Often considered an antioxidant, biochemical and in vitro data indicate that noncrystalline, soluble uric acid also can react to form radicals, increase lipid oxidation, and induce various pro-oxidant effects in vascular cells. In vitro and in vivo findings suggest that uric acid may contribute to endothelial dysfunction by inducing antiproliferative effects on endothelium and impairing nitric oxide production. Proinflammatory and proliferative effects of soluble uric acid have been described on vascular smooth muscle cells (VSMCs), and in animal models of mild hyperuricemia, hypertension develops in association with intrarenal vascular disease. Possible adverse effects of uric acid on the vasculature have been linked to increased chemokine and cytokine expression, induction of the renin-angiotensin system, and to increased vascular C-reactive protein (CRP) expression. Experimental evidence suggests a complex but potentially direct causal role for uric acid in the pathogenesis of hypertension and atherosclerosis.
Gov't Doc #: 15660333
Type: Journal Article
Subjects: Animals
Biological Markers.blood
Disease Progression
Endothelium, Vascular.metabolism.pathology.physiopathology
Uric Acid.blood
Vascular Diseases.blood.pathology.physiopathology
Appears in Collections:Journal articles

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