子宫内膜纤维化是宫腔粘连最显著特征，主要病理生理过程为上皮间质转化，而间质上皮转化作为其逆反过程参与子宫内膜再生修复。因此明确子宫内膜间质上皮转化过程，对抑制子宫内膜纤维化促进修复至关重要。我们前期研究发现子宫内膜间充质干细胞(eMSC)可使子宫内膜间质细胞纤维化因子α-SMA、collagen I表达下调，上皮性标记cytokeratin表达上调，提示eMSC具有促进间质上皮转化、抑制子宫内膜纤维化作用，但其具体作用机制尚不清楚。Hippo/TAZ信号通路在调控上皮间质转化及α-SMA表达中有关键作用，而且在子宫内膜中呈特异性时空表达，提示Hippo/TAZ信号通路很可能是eMSC在抑制子宫内膜纤维化中的重要机制。本项目拟从体内和体外实验进行深入研究，阐明Hippo/TAZ信号通路介导的间质上皮转化在eMSC抑制子宫内膜纤维化中的作用机制，为宫腔粘连的治疗提供新的的理论基础和潜在靶点。

Endometrial fibrosis has been implicated in the development of intrauterine adhesion, which is characterized by epithelial mesenchymal transition (EMT). As a reverse process of EMT, mesenchymal epithelial transition (MET) involves in endometrial regeneration. So it is important to understand the process of MET for prevention of endometrial fibrosis. We found that the expressions of α-SMA and collagen I in endometrial stromal cells were down regulated by endometrial mesenchymal stem cells (eMSC), while the expression of cytokeratin was up-regulated. It suggested that eMSC could promote MET and prevent endometrial fibrosis. The Hippo/TAZ signal pathway plays an important role in regulating EMT process and the expression of α-SMA. Meanwhile, it shows a specific temporal and spatial expression in endometrium. These imply that Hippo/TAZ signal pathway is important for eMSC to inhibit endometrial fibrosis. In this study, we plan to clarify the mechanism of eMSC in preventing endometrial fibrosis in vivo and in vitro. Our research will provide a new strategy for the treatment of intrauterine adhesion.