In contrast, rhACE2 treatment appeared to show counter regulation against Ang II-mediated kidney inflammation, oxidative stress and renal injury by augmenting renal Ang-(1-7) levels, enhancing nephrin expression, and preventing the activation of NOX4 and TNF-α-TNFRSF1A signaling and these mechanisms may be involved in the therapeutic benefits of ACE2 in the ApoE-deficient mice. Here, AGT is linked to nephritis.