BDKRB2 and renal fibrosis: However, the role of ACE inhibition and bradykinin B2 signaling pathway activation is still controversial because it was also shown that ACE-I treatment in the UUO model using either bradykinin B2 receptor knockout mice or control mice demonstrated that ACE-I exhibited a significant reduction in renal fibrosis in all groups [116], suggesting that the presence of bradykinin B2 receptor signaling may not be necessary for the tissue protection mediated by ACE-I in this model [116].