http://hdl.handle.net/1765/24983

pubmed: 19404405
scopus: 65549108738



Angiotensin-(1-7) and the G protein-coupled receptor Mas are key players in renal inflammation


Article
volume 4, issue 4.
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Angiotensin (Ang) II mediates pathophysiologial changes in the kidney. Ang-(1-7) by interacting with the G protein-coupled receptor Mas may also have important biological activities. In this study, renal deficiency for Mas diminished renal damage in models of renal insufficiency as unilateral ureteral obstruction and ischemia/reperfusion injury while the infusion of Ang-(1-7) to wild-type mice pronounced the pathological outcome by aggravating the inflammatory response. Mas deficiency inhibited NF-κB activation and thus the elevation of inflammation-stimulating cytokines, while Ang-(1-7) infusion had proinflammatory properties in experimental models of renal failure as well as under basal conditions. The Ang-(1-7)-mediated NF-κB activation was Mas dependent but did not involve Ang II receptors. Therefore, the blockade of the NF-κB-activating properties of the receptor Mas could be a new strategy in the therapy of failing kidney.





Automatically Extracted Terms
  • kidney
  • figure
  • nf-kb
  • receptor
  • wild-type
  • animal
  • angiotensin
  • control
  • inflammation
  • wild-type mice
  • effect
  • ang ii receptors
  • wild-type controls
  • proinflammatory
  • mas-deficient mice
  • disease
  • activation
  • mas-deficient
  • pathomorphological changes
  • infusion


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