胚胎着床是妊娠成功的第一步，大约75%的早期妊娠丢失是由于胚胎着床障碍所致，其中，子宫内膜容受性异常是主要原因，但其具体分子机制目前仍不清楚。胚泡着床的过程主要依靠细胞与细胞、细胞基质之间的相互粘附作用，所以研究细胞粘附相关分子是了解胚胎着床机制的关键。前期工作中，我们发现在女性黄体中期宫腔粘液中细胞粘附功能相关的talin1表达量较高，随后的小鼠实验中也证实talin1在内膜中呈时空性表达以及妊娠时期高表达。提示talin1蛋白在胚胎着床过程中可能发挥重要的作用。因此，本研究拟继续通过细胞水平和动物模型探究talin1在激活整合素通路、FKA通路中的作用，并挖掘talin1蛋白在胚胎着床过程所调控的具体分子和信号通路。本研究有助于我们从新的视角理解胚胎着床的机制，为临床上探索子宫内膜容受性新分子标志和改善子宫内膜容受性的治疗方法提供实验依据。

Embryo implantation is the first step of pregnancy success, however， approximately 75% of early pregnancy loss wereattributed to embryo implantation failure. Endometrial receptivity abnormalities were the main causes of embryo implantation defect, but the underlying molecular mechanismswere still largely unclear. The process of blastocyst implantation was mainly based on the mutual adhesion between cells and cell matrix. During previous study, we found that the expression of cell adhesionassociated factor talin1 was expression high in intrauterine mucus in patients with repeated implantation failure. Later, animal experiments also showed that talin1 was highlyexpressedduring early pregnancy, which suggested that talin1 protein may play a crucial role in embryo implantation. This study intended to explore the regulation of talin1inintegrin pathway and FKA pathwayassociated proteins at cellular level and animal models, and to explore the specific molecular and signaling pathways mediated by talin1 protein during implantation. This study will broadenour understandingof the mechanismsunderlying embryo implantation, and provide an experimental evidence for clinical exploration of new molecular markers of endometrial receptivity.