Fig. 10

Effects and potential mechanisms of ACE2 on renal inflammation and injury in ApoE-deficient mice. ACE2 serves as a key regulator of Ang II-mediated actions in kidneys. On one hand, ACE2 deficiency results in downregulation of nephrin levels and greater increases in ROS production and expression of proinflammatory cytokines TNFα, IL-1, IL-6, and IL-17A, contributing to renal inflammation, oxidative stress and structural injury in the ApoEKO mice. On the other hand, rhACE2 treatment promotes nephrin levels and ameliorates the Ang II-induced kidney inflammation and ROS generation, functioning as a negative regulator for kidney dysfunction and renal injury in the ApoEKO mice.