AGT and Myocardial fibrosis: Physiologically, ACE-2 catalyzes the conversion of angiotensin II to angiotensin (1–7), with vasodilator-related, anti-inflammatory, and antifibrotic effects on the respiratory system, in addition to inducing antioxidant stress [82], protecting against the effects of excessive activation of the ACE–Ang-II–AT1R axis [82], with proinflammatory and profibrotic effects in the respiratory system, and causing vascular dysfunction, myocardial fibrosis, nephropathy, and RAAS insulin resistance [82].