The stimulation of the ACE2/Ang-(1-7)/Mas axis has been successful used to prevent and reverse PH and fibrosis in animals. ACE2 activation using the compound XNT or induction of ACE2 overexpression by gene transfer efficiently prevented and, more importantly, reversed the increase of the right systolic ventricular pressure (RSVP), pulmonary fibrosis, imbalance of the RAS, and inflammation in animals (rats and mice) with PH induced by monocrotaline (MCT) or in rats with pulmonary fibrosis caused by bleomycin treatment [39, 117, 118] . In keeping with these findings, Ang-(1-7) gene transfer into the lungs triggered similar protective actions in MCT-treated rats [39] . In addition, Ang-(1-7) via Mas prevented the apoptosis of alveolar epithelial cells and the Jun N-terminal kinase (JNK) activation induced by bleomycin [122] . The involvement of the Ang-(1-7)/Mas in PH was further evidenced by the observation that the XNT effects are blocked by A-779 [117] . Furthermore, in both lung specimens from patients with idiopathic pulmonary fibrosis and from animals with bleomycin-induced pulmonary fibrosis were reported a reduction in mRNA, protein, and activity of ACE2 with a reciprocal increase in Ang II level [116] .