Since ACE/Ang II/AT1R axis hyperactivity is known to cause renal injury by accelerating renal fibrosis, inflammation, and oxidative stress, which is also found in AS, the ability of Ang-[1–7] administration to activate the ACE2/Ang-[1–7]/Mas receptor axis ultimately protected against renal injury in experimental AS. Here, ACE is linked to renal fibrosis.