ase neprilysin (17), although with less favorable kinetics at baseline. Thus, it can be assumed ACE inhibitors disrupt the balance between catalytically active ACE and ACE2, resulting in favored activation of the ACE2/Ang1-7/Mas axis.
Overall, because of the demonstrated anti-inflammatory, antifibrotic, and antithrombotic effects associated with the ACE2/Ang1-7/Mas axis, upregulation could serve as a