The ACE/Ang II/AT1R axis is upregulated in PAH and has been linked to the deleterious cardiopulmonary effects observed in PAH, promoting aberrant proliferation, migration, resistance to apoptosis, vasoconstriction, hypertrophy, inflammation, fibrosis, and oxidative stress, all of which enhance the abnormal vascular remodeling process in the pulmonary artery [6,11,12,13,14,15,16,17]. Here, AGT is linked to pulmonary arterial hypertension.