MAS1 and renal fibrosis: While Pinheiro et al (2009) [16] showed that the genetic deletion of Mas receptor in C57Bl/6 background mice led to glomerular hyperfiltration, proteinuria and renal fibrosis, Esteban et al (2009) [17] reported that renal deficiency of Mas diminished renal damage in unilateral ureteral obstruction and ischemia/reperfusion injury, and that the infusion of Ang-(1–7) to wild-type mice elicited an inflammatory response.