CCND1 and acute kidney injury: Furthermore, western blot analysis demonstrated that exogenous expression of miR-214 inhibited the protein level of DKK3 and promoted β-catenin, c-myc, and cyclin D1 levels in I/R-induced rat AKI model when compared with that in sham group (Fig. 5f), suggesting that miR-214 activated the Wnt/β-catenin pathway by targeting Dkk3. These data demonstrated that miR-214 ameliorated AKI in vivo by repressing apoptosis through targeting Dkk3 and activating Wnt/β-catenin pathway.