Objective: HK-2 were divided into five groups for study as follows: normal; UA; UA+Fasudil; UA+ROCK1 si-RNA; UA+sc-siRNA. To measure Rho-kinase activity,mitochondrial oxidative injury and apoptosis-related protein of each group. T test was adopted to analysis the difference between groups. Methods: Overexpression of MYPT1 were shown in HK-2 cells induced by UA. High uric acid treatment also up-regulated the expression of Rho-kinase activity,mitochondria and apoptosis-related protein,while treatment with Fasudil and ROCK1 si-RNA significantly attenuated these response. Results: Rho-kinase signal pathway participates in the tubular mitochondrial oxidative injury and apoptosis via regulating mitochondrial dyneins/biogenic genes in uric acid nephropathy,which suggests that mitochondria pathway may represent a potential therapeutic target for hyperuricemia nephropathy. Conclusions: Objective: Oxidative stress is a pathologic feature of hyperuricemia which is highly prevalent and contributes to kidney tubular interstitial fibrosis. Rho-kinase is closely related to oxidative stress induced by mitochondria. Here,we designed to explore the expression and role of Rho-kinase in hyperuricemia nephropathy. Secondary objective were to investigate whether the Rho-kinase signal pathway regulated the hyperuricemic tubular oxidative injury and apoptosis via mitochondrial pathway and the mechanisms involved. Methods: HK-2 were divided into five groups for study as follows: normal; UA; UA+Fasudil; UA+ROCK1 si-RNA; UA+sc-siRNA. To measure Rho-kinase activity,mitochondrial oxidative injury and apoptosis-related protein of each group. T test was adopted to analysis the difference between groups. Results: Overexpression of MYPT1 were shown in HK-2 cells induced by UA. High uric acid treatment also up-regulated the expression of Rho-kinase activity,mitochondria and apoptosis-related protein,while treatment with Fasudil and ROCK1 si-RNA significantly attenuated these response. Conclusions: Rho-kinase signal pathway participates in the tubular mitochondrial oxidative injury and apoptosis via regulating mitochondrial dyneins/biogenic genes in uric acid nephropathy,which suggests that mitochondria pathway may represent a potential therapeutic target for hyperuricemia nephropathy.