IgA肾病是全球最常见的原发性肾小球疾病。低糖基化IgA1免疫复合物沉积于肾小球致系膜细胞增殖是其早期主要病理特征,具体机制未明。我们预实验发现IgA肾病小鼠模型肾组织中miR-214-3p及eIF3d表达增加。结合前期研究我们推测：多聚低糖基化IgA1免疫复合物沉积于肾小球系膜区，致miR-214-3p表达增加，通过抑制PTEN表达活化JNK/c-Jun通路，加快细胞周期转换,促进IgA肾病系膜细胞增殖；同时c-Jun与eIF3d在转录水平及转录后水平交互作用，形成eIF3d与c-Jun正反馈环路促进系膜细胞增殖，造成肾脏损伤。本项目拟从体内体外两个层次开展研究，采用荧光素酶报告基因系统、miRNA模拟/抑制物、慢病毒载体等技术，探索miR-214-3p通过eIF3d与PTEN/JNK/c-Jun交互作用参与IgA肾病发病机制，为IgA肾病防治提供新的理论依据与治疗靶点。

IgA nephropathy(IgAN) is the most prevalent primary chronic glomerular disease worldwide. Its early pathological change is characterized by mesangial cell proliferation induced by deposition of polymeric Galactose-deficient IgA1 immune complex, while its regulatory mechanism remains unclear. Our experiments showed that miR-214-3p and eIF3d were upregulated in kidneys of IgAN mouse model. According to previous studies, we propose that miR-214-3p inhibiting PTEN, which regulates mesangial cell proliferation in IgAN through eIF3d specified interacting with c-Jun in JNK/c-Jun pathway, induced by polymeric Galactose-deficient IgA1 immune complex.Interaction between eIF3d and c-Jun in the transcriptional and posttranscriptional level creates a positive feedback loop contributing to mesangial cell proliferation in IgAN. Based on the in vitro and in vivo studies, we aim to explore how miR-214-3p involve in the pathogenesis of IgA nephropathy through the interaction between eIF3d and PTEN/JNK /c-Jun pathway by experimental techniques of luciferase reporter system, miRNA mimic/inhibitor and lentivirus transfection. This study would provide theoretical basis and therapeutic target for prevention and treatment of IgAN.