Objective To explore the mechanism of mitochondria in hypertensive vascular endothelial cell injury on based on the HUR/PIM1 signaling pathway. Methods HUVCE cells treated with different concentrations of AngⅡ were divided into three groups：a control group，AngⅡ group and Mdivi⁃1 group. Cell viability，apoptosis and migration rate were detected by CCK8，flow cytometry and Transwell. Mitochondrial ⁃ selective probes were used todetect mitochondrial morphology，and JC⁃1 dye was applied to measure mitochondrial membrane potential. Contents of intracellularDrp ⁃1，ROS，HUR/PIM1 mRNA and protein were detected by qPCR and Western blot， and angiogenesis was verified by angiogenesis in vitro. Results As compared with the control group，the AngⅡ group cell viability was decreased，expressions of Drp⁃1 and ROS proteins were increased，mitochondrial morphology was changed，membrane potential was declined，contents of mRNA and protein were enhanced in theHUR/PIM1 signaling pathway，and angiogenesis was increased. The effect of Mdivi ⁃1 group wason the contrary. Conclusions Mdivi⁃1 reduces mitochondria expression and expression of HUR/PIM1 pathway in AngⅡ⁃induced cells，and inhib⁃ its the apoptosis，migration and angiogenesis of AngⅡ⁃induced cells.
