Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9855
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dc.contributor.authorKanellis, Johnen
dc.contributor.authorKang, Duk-Heeen
dc.date.accessioned2015-05-15T23:07:12Z
dc.date.available2015-05-15T23:07:12Z
dc.date.issued2005-01-01en
dc.identifier.citationSeminars in Nephrology; 25(1): 39-42en
dc.identifier.govdoc15660333en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9855en
dc.description.abstractRecent 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.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherArteries.metabolism.pathology.physiopathologyen
dc.subject.otherBiological Markers.blooden
dc.subject.otherDisease Progressionen
dc.subject.otherEndothelium, Vascular.metabolism.pathology.physiopathologyen
dc.subject.otherHumansen
dc.subject.otherHyperuricemia.blood.pathology.physiopathologyen
dc.subject.otherUric Acid.blooden
dc.subject.otherVascular Diseases.blood.pathology.physiopathologyen
dc.titleUric acid as a mediator of endothelial dysfunction, inflammation, and vascular disease.en
dc.typeJournal Articleen
dc.identifier.journaltitleSeminars in nephrologyen
dc.identifier.affiliationDepartment of Nephrology and Medicine, University of Melbourne, Austin Hospital, Australiaen
dc.description.pages39-42en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/15660333en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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