在体外受精-胚胎移植中，反复薄型内膜常导致多次移植周期取消及反复种植失败，目前仍缺乏有效治疗手段。前期临床研究中，我们首次发现宫腔灌注粒细胞巨噬细胞集落刺激因子（GM-CSF）可有效增加反复薄型内膜患者的内膜厚度，显著提高临床妊娠率和种植率，但其具体机制不详。前期基础研究发现GM-CSF可增加反复薄型内膜患者内膜基质细胞的增殖及迁移，并上调子宫内膜容受性相关基因HOXA10及下游整合素β3（ITGβ3）的表达水平。基于此，我们推测GM-CSF可能通过激活特定信号通路上调HOXA10/ITGβ3表达，进而改善子宫内膜容受性。因此，本课题将从原代细胞、动物模型以及临床水平研究以下科学问题：GM-CSF是否以及如何通过上调HOXA10/ITGβ3，进而改善子宫内膜容受性并提高临床妊娠率？本研究将揭示GM-CSF改善子宫内膜容受性的分子机制，为反复薄型内膜患者提供新的治疗策略及相关理论支持。

Persistent thin endometrium positively correlates with the risk of embryo transfer cycle cancellation and repeated implantation failure in vitro fertilization-embryo transfer (IVF-ET). It’s urgent to explore the effective clinical therapy for persistent thin endometrium. Notably, in our preliminary clinical studies, we firstly identified that intrauterine infusion of granulocyte macrophage colony stimulating factor (GM-CSF) increased the endometrial thickness, and then improved implantation rate and clinical pregnancy rate in the patients with persistent thin endometrium. However, the underlying mechanism is still unclear. Endometrial stroma cells were isolated from patients with persistent thin endometrium and then cultured in vitro. The results from CCK8 and migration assays showed that GM-CSF dramatically enhanced cell proliferation and migration. Additionally, GM-CSF notably elevated the expression levels of endometrial receptivity associated gene, homeobox A10 (HOXA10), which is critical for endometrial receptivity (ER), and its target, integrin subunit beta 3 (ITGβ3). Therefore, we hypothesized that GM-CSF increases HOXA10/ITGβ3 levels to promote endometrial cell proliferation and ER improvement. In the present study, we aim to verify the correlation between GM-CSF and ER improvement and identify the molecular mechanism of GM-CSF/HOXA10/ITGβ3 in improving ER by using primary cells, animal models and clinical samples analyses. Our study may provide promising therapeutic strategies for patients with persistent thin endometrium.