MAS1 and pulmonary arterial hypertension: In accordance with the findings of Ferreira and colleagues [61], beneficial effects of ACE2 activation in PAH seem to be at least partly mediated through angiotensin-(1–7)/Mas axis, since improvements of mean PAP, RV hypertrophy, pulmonary vasorelaxation, and neointimal formation were all abolished by the Mas antagonist A779 [64].