Abstract: Ｏｂｊｅｃｔｉｖｅ：To investigate the role of A kinase anchor protein 1 (AKAP1) in renal ischemia reperfusion injury (IRI) and its mechanism.
Ｍｅｔｈｏｄｏｌｏｇｙ：The mouse renal ischemia reperfusion model was established by bilateral renal arteries clamped for 28 min of ischemia. After 24 h of reperfusion, blood samples were collected and kidney tissues were retained to detect serum creatinine, urea nitrogen, pathological injury and AKAP1 expression;Then the mouse proximal tubule cells were cultured to the second day for intervention of hypoxia (H). The cells were placed into a three-gas incubator with 1％O2, 5％ CO2, 37 ℃ and were cultured without sugar or serum successively for 3h. Then the cells were reoxygenated (R) and replaced with lowglucose DMEM containing 10％ fetal bovine serum for normal culture for 6h. The general morphology of renal tubule cells in control group and each H／R group were observed after reoxygenation for 6h. Finally, ATP content, mitochondrial membrane potential and mitochondrial MitoRed staining in each H／R group were detected by transfection with AKAP1 overexpression.
Ｒｅｓｕｌｔｓ：AKAP1 expression decreased after renal ischemia reperfusion (P<0.05). AKAP1 expression was decreased and mitochondrial dysfunction was observed in renal tubular epithelial cells after deoxygenation (P<0.05). AKAP1 induced mitochondrial damage through Drp1 regulation of hyporexia (P<0.05).
Ｃｏｎｃｌｕｓｉｏｎ：AKAP1 reduce renal ischemiareperfusion injury by inhibiting mitochondrial dysfunction.

Key words: kinase anchor protein 1, acute kidney injury, ischemia reperfusion injury, mitchondrial division, dynamin-related protein 1