Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9354
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dc.contributor.authorCao, Zeminen
dc.contributor.authorCooper, Mark Een
dc.date.accessioned2015-05-15T22:25:14Z
dc.date.available2015-05-15T22:25:14Z
dc.date.issued2001-11-01en
dc.identifier.citationSeminars in Nephrology; 21(6): 554-62en
dc.identifier.govdoc11709803en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9354en
dc.description.abstractThe renin angiotensin system (RAS) has been implicated in tubulointerstitial injury in a range of clinical and experimental settings. Angiotensin II, the major effector molecule of the RAS, in addition to its effects on systemic blood pressure and intrarenal hemodynamics, also acts as a local hormone and growth factor to modulate renal function and pathology. There is increasing evidence for a pivotal role of this hormone in influencing renal tubular and interstitial function and structure including regulation of multiple cytokines and chemokines, promoting infiltration of monocytes/macrophages, promoting cellular proliferation, and inducing apoptosis. Pathologic actions of angiotensin II lead to tubulointerstitial fibrosis and inflammation via a range of cytokines and chemokines including transforming growth factor (TNF)-beta1, osteopontin, tumor necrosis factor (TNF)-alpha, secreted protein acidic and rich in cysteine (SPARC), and RANTES (regulated on activation normal T-cell expression and secreted). Blockade of production of angiotensin II by an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor antagonism with an angiotensin type 1 receptor antagonist has been shown to attenuate tubulointerstitial injury and reduce expression of cytokines and matrix proteins. The role of angiotensin II in tubulointerstitial fibrosis and inflammation is addressed in this article.en
dc.language.isoenen
dc.subject.otherAngiotensin II.physiologyen
dc.subject.otherAnimalsen
dc.subject.otherChemokine CCL5.physiologyen
dc.subject.otherCytokines.physiologyen
dc.subject.otherHumansen
dc.subject.otherKidney Tubules.physiologyen
dc.subject.otherNF-kappa B.physiologyen
dc.subject.otherNephritis, Interstitial.metabolism.pathologyen
dc.subject.otherOsteonectin.physiologyen
dc.subject.otherOsteopontinen
dc.subject.otherRenin-Angiotensin System.physiologyen
dc.subject.otherSialoglycoproteins.physiologyen
dc.subject.otherTransforming Growth Factor beta.physiologyen
dc.subject.otherTransforming Growth Factor beta1en
dc.subject.otherTumor Necrosis Factor-alpha.physiologyen
dc.titleRole of angiotensin II in tubulointerstitial injury.en
dc.typeJournal Articleen
dc.identifier.journaltitleSeminars in nephrologyen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin, Australiaen
dc.description.pages554-62en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/11709803en
dc.type.austinJournal Articleen
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
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