Abstract: Ｏｂｊｅｃｔｉｖｅ：To study the role and mechanism of protein phosphatase PHLPP2 in  development of acute kidney injury (AKI); Ｍｅｔｈｏｄｏｌｏｇｙ：Wild type C57BL/6 (WT) and knockout PHLPP2（PHLPP2-/-） mice were divided into WT control group,WT cisplatin (CDDP) treatment group,PHLPP2-/- control group and PHLPP2-/- CDDP treatment group (10 mice in each group) to establish AKI model.Three days later,the mice were killed.The mRNA and protein levels of PHLPP2 were detected by RTPCR and Western Blot; HE and TUNEL staining were used to detect renal tissue damage and cell apoptosis,renal tubular epithelial cells (RTECS) were isolated and identified; JC1 method was used to detect the changes of mitochondrial membrane potential; The protein levels of Bax,Caspase3,and Bcl2 and the phosphorylation levels of Thr308 and Ser473 in AKt Kinase were detected by Western Blot assay.Ｒｅｓｕｌｔｓ：In AKI model induced by CDDP,expression of PHLPP2 in kidney tissue was significantly increased; compared with WT CDDP group,renal tissue structure damage and apoptosis were alleviated.Mitochondrial structure damage was reduced,and mitochondrial membrane potential was decreased; Knockout of PHLPP2 gene could significantly promote expression of Bcl2 protein,but inhibit expression of Bax and caspase3.PHLPP2 gene regulated expression of these proteins through dephosphorylation of thr308 and ser473 of Akt.Ｃｏｎｃｌｕｓｉｏｎ：Knockout of PHLPP2 can protect normal structure and function of mitochondria by alleviating the decline of mitochondrial membrane potential,thus improving AKI injury through mitochondrial apoptosis.