aPC具有肾脏保护作用，其在IMN中的作用未知。YB-1是核转录因子之一。前期运用UCSC基因库查找生物信息时发现，人及大鼠PLA2R基因启动子中均存在Y盒。我们预实验发现，与正常大鼠相比，PLA2R在YB-1-/+大鼠肾脏组织中表达量下降，在YB-1+/+大鼠肾脏组织中表达量上升。这说明YB-1可通过绑定基因启动子促进PLA2R转录。前期运用软件PhosphoNETKinase Predictor证实ERK1/2可介导YB-1磷酸化。因此，我们假设：在PLA2R相关性IMN时，aPC通过激活ERK1/2介导YB-1磷酸化，磷酸化的YB-1与基因启动子结合抑制PLA2R基因转录激活。我们将采用Real-time PCR、Western blot、慢病毒转染等手段分别从细胞、组织及整体动物水平等方面探讨aPC通过YB-1参与PLA2R相关性IMN发病机制，为IMN的防治提供理论基础。

APC plays a renoprotcetive role in kidney diseases, although, little article reports the function and mechanism of aPC in IMN.The role of YB-1 in kidney diseases is controversy, and there is seldom literature about the relationship between YB-1 and IMN. Previously, we find that there is Y box in promoter of human and mouse PLA2R gene using UCSC database. Our previous experiment confirm that the expression of PLA2R is decreased in YB-1-/+ mouse, and the expression of PLA2R is increased compared with normal C57BL/6 mouse, which means YB-1 can bind to the promoter of PLA2R gene to facilitate the expression of PLA2R.Besides, PhosphoNETKinase Predictor suggests that ERK1/2 can induce YB-1 phospholation. Therefore, we hypothesized that aPC plays an inhibition role in transcription of PLA2R gene via phosphorylating YB-1 induced by ERK1/2. We will explore the mechanism from cell, tissue and animal model through Real-time PCR, Western blot and Lentivirus transfection et al. and provide the theoretical basis and experimental evidence for the prevention and treatment of PLA2R related IMN.