足细胞损伤是乙肝相关性肾炎（HBV-GN）发病及进展的重要原因。研究报道细胞焦亡是促炎症介质释放的主要形式，在我们前期研究中发现HBV-GN存在足细胞焦亡，以及NLRP3炎症小体及其下游炎症因子表达水平的增高，通过基因芯片及RT-PCR发现miR-223表达水平下调。进一步生物信息学提示NLRP3是miR-223靶基因。我们推测，miR-223通过调控靶基因NLRP3介导HBV-GN足细胞焦亡。本研究以HBx为诱因，首先通过体内外实验进一步验证NLRP3炎症小体信号通路与足细胞焦亡的关系；其次鉴定miR-223的靶基因NLRP3；最后通过过表达及基因沉默，分别在体外和体内水平观察miR-223对NLRP3炎症小体信号通路及足细胞焦亡的影响，为阐明HBV-GN足细胞损伤机制提供新的理论依据，为临床防治寻找新的干预靶点。

Podocyte injury has been identified as a key word resulting in hepatitis B virus-associated glomerulonephritis(HBV-GN), Which contributes to HBV-GN development and progression. Recent studies indicate that pyroptosis leads to the release of pro-inflammatory cytokines. We have recently found podocyte pyroptosis, high expression of NLRP3 inflammasome and downstream inflammatory cytokines in HBV-GN. We also find low expression of miR-223 by miRNAs differential expression chips and real time-PCR. Bioinformatics prediction indicates that miR-223 may regulate the expression of NLRP3. Therefore, we propose that miR-223 is involoved in podocyte pyroptosis in HBV-GN by regulating NLRP3 inflammasome singling pathway. HBx transgenic mice is used to verify this hypothesis, we intend to carry out the project from three aspects. Firstly, we evaluate the relationship between NLRP3 inflammasome singling pathway and podocyte pyroptosis in vivo and vitro. Secondly, we verify NLRP3 as target gene regulated by miR-223. Finally, the influence of miR-223 regulating NLRP3 pathway to podocyte pyroptosis will be further investigated by using gene transfection or RNA interference. Better understanding of podocyte pyroptosis wil not only give insight into disease pathogenesis, but can also lead to development of new therapeutic strategies for treatment of HBV-GN.