| First Author | Esteban V | Year | 2009 |
| Journal | PLoS One | Volume | 4 |
| Issue | 4 | Pages | e5406 |
| PubMed ID | 19404405 | Mgi Jnum | J:148250 |
| Mgi Id | MGI:3844151 | Doi | 10.1371/journal.pone.0005406 |
| Citation | Esteban V, et al. (2009) Angiotensin-(1-7) and the g protein-coupled receptor MAS are key players in renal inflammation. PLoS One 4(4):e5406 |
| abstractText | 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-kappaB 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-kappaB activation was Mas dependent but did not involve Ang II receptors. Therefore, the blockade of the NF-kappaB-activating properties of the receptor Mas could be a new strategy in the therapy of failing kidney. |
