胚胎着床过程中母胎相互作用关键调控通路异常将致复发性流产、子痫前期等妊娠疾病。通道蛋白及其分子调控网络在母胎细胞对话中发挥重要作用，但进一步的分子机制及其与妊娠疾病的关系尚不清楚。本课题在前期已发现通道蛋白ENaC参与母胎互作的基础上，将利用高通量组学、生物信息学及分子生物学技术，结合临床标本、细胞模型以及条件性基因敲除小鼠，明晰关键离子通道、水通道蛋白等在子宫内膜容受建立和维持中的作用机制，研究离子通道蛋白（如ENaC、BKCa）、水通道蛋白在母胎识别、胚胎植入及子宫基质-蜕膜转化和重塑过程中的作用及其受母体内分泌、胚胎源性因子旁分泌、自分泌调控的分子网络机制，探索胚胎着床过程中母胎互作关键调控通路与复发性流产和子痫前期等妊娠疾病发生的关联性及时序性，发现妊娠疾病共同风险因子和生物标记物，为妊娠疾病发生的分子机制溯源研究提供理论基础，为临床进行疾病早期预警、风险评估和源头干预提供新策略。

The abnormal key regulatory pathways in maternal-fetal interaction during the process of embryo implantation could induce recurrent abortion, preeclampsia and other pregnancy diseases. Channel proteins and their molecular regulatory networks play an important role in maternal-fetal cellular cross-talk. However, the further molecular mechanism and its relationship with pregnancy diseases are not clear. Based on our previous finding that the channel protein ENaC participates in maternal-fetal interaction, we will use high-throughput omics, bioinformatics and molecular biology technology, combined with the clinical specimens, cell model and conditional gene knockout mice, to clarify the mechanism of key ion channel and water channel proteins in endometrial receptivity establishment and maintenance; study the role of ion channel proteins (such as ENaC, BKCa), the water channel proteins in maternal fetal recognition, embryo implantation and uterine stromal decidual transformation and reshaping, and, the molecular network mechanisms by maternal endocrine regulation and paracrine, autocrine regulation of embryo-derived factors; explore the relationship between key regulatory pathways of maternal-fetal interactions during embryo implantation and recurrent abortion, preeclampsia and other pregnancy diseases; find the common risk factors and biomarkers of pregnancy diseases; supply a theoretical basis for research on the origin of the molecular mechanism of pregnancy diseases; provide new strategies for early warning, risk assessment and source intervention of the clinical diseases.