ACE and pulmonary fibrosis: On the other hand, the conversion of Ang II into Ang 1-7 by ACE2 counteracts the action of Ang II in pulmonary fibrosis, so that a depletion of ACE increases collagen deposits in the extracellular matrix, resulting in an imbalance between ACE/ACE2 that has been related to the severe progression of respiratory diseases (68), as seen in patients with chronic obstructive pulmonary disease, where there is greater ACE activity (60).