ACE2 and pulmonary fibrosis: Angiotensin1-7 (Ang-(1–7), a heptapeptide) is generated directly via the conversion of Ang-II by ACE-2 or indirectly via Ang-I by ACE-2 and ACE.28 Binding of Ang-II to Angiotensin type-1 receptor (AT-I) leads to vasoconstriction, proliferation, and fibrosis in multiple tissues, whereas binding of Ang-(1–7) to the MAS receptor induces vasodilation, inhibiting fibrosis, thrombogenesis, hypertension, cardiac hypertrophy and lung fibrosis.28,30–33 The balance between the opposing effector molecules Ang-II and Ang-(1–7) may play a pivotal role in tissue injury and recovery.