Figure 1. . Schematic representation of ACE2 within the renin–angiotensin–aldosterone pathway.

Once infected, it is likely that augmentations of ACE2 and Ang(1–7) will be protective for the cardiac and pulmonary systems. In contrast Ang-II and the Type 1 receptor of Ang-II have been shown to be destructive to the cardiac system and result in pulmonary leakage and fibrosis.