慢性肾脏病的防治是世界范围内的公共卫生问题。近年来的临床研究发现他汀具有肾脏保护作用，通过基础研究已经初步明确他汀通过抑制小G蛋白Rac、Rho等在肾脏发挥多效保护作用。但是他汀对维护正常肾小球滤过功能的足细胞的保护作用和作用机制还知之甚少。同时，最近的研究发现Rac1持续活化能导致足细胞的表型改变，如足突融合、细胞凋亡等，进而导致肾小球纤维化。本研究拟通过在体动物模型研究Rac1在他汀保护足细胞表型改变以过程中的作用和作用机制；通过体外细胞实验研究Rac1在他汀及对足细胞运动能力、细胞骨架重排的影响和作用机制。通过本研究将对全面认识他汀的器官保护这一多效性作用机制提供理论依据，对进一步研究慢性肾脏病的防治策略提供新的思路。

The prevention and treatment of chronic kidney disease is a worldwide public health problem. In recent years, clinical studies found that statins have renoprotective effects, basic research has been initially clear protective effect of statins play multi-effect through the inhibition of small G proteins of Rac, Rho, in the kidney. Statins protective role and mechanism of action for the maintenance of normal glomerular filtration rate podocytes is also poorly understood. At the same time, recent studies have found that sustained Rac1 activation energy lead to phenotypic changes of podocytes and foot process fusion, apoptosis, leading to glomerular fibrosis.In this study, intended by the body of animal model studies Rac1 in his statins protect the foot cell phenotype change by in vitroexperimental study Rac1 to the process of role and the role of mechanisms; statins and foot cell movement ability, cytoskeletonrearrangement influence and role mechanism. This pleiotropic mechanism of statin organ protection by the comprehensiveunderstanding of this study will provide a theoretical basis to provide new ideas for further study of chronic kidney diseaseprevention and control strategies.