Objective:To investigate the effects of scarred uterus on endometrium receptivity and invasion of placental trophoblasts using a mouse model.Methods:A scarred uterus mouse model was established on 30 female Specific Pathogen Free mice. Full-layer incision on unilateral uteruses was performed simulating a cesarean section to establish the scarred uterus mice model and the contralateral uteruses were used as control. The number of implanted blastocysts between the scarred and non-scarred uteruses was compared at 4.5 d after conception (windows of implantation, WOI). The morphology of pinopod was observed under electron microscopy, and the expression of endometrial receptivity-related molecules, such as leukemia inhibitor factor (Lif) and mucin-1 (MUC1), and mRNA of Lif and MUC1 were analyzed by immunohistochemistry and reversed transcription-polymerase chain reaction technique, respectively. During the placental formation period (day 13.5, 15.5, and 17.5 after conception), the development of the decidual layer, junction layer, and labyrinth layer of the placenta were observed under microscope, and the distribution of glycogenotrophoblast cells and the location of CK7-traced invasion trophoblasts were determined with immunohistochemistry. Paired t test and one-way analysis of variance were used for statistical analysis. Results:Compared with the control side, the number of blastocysts implantation on the scarred uterus decreased significantly at 4.5 d after conception (3.50±0.54 vs. 1.33±0.81, t=7.05, P=0.001). In the WOI, the scarred uteruses were found to have decreased scores of endometrial pinopodes coverage (1.60±0.44 vs. 2.75±0.28, t=15.06, P<0.001), decreased mRNA expression of Lif (0.71±0.12 vs. 1.49±0.30, t=5.16, P=0.004) and increased MUC1 mRNA [(2.19±0.45) vs.(1.03±0.17), t=7.51, P<0.001] comparing with the control. No significant changes in the area and general morphology were observed in the three different layers on either side during the placental formation period. In terms of trophoblast invasion, the grayscales of glycogen trophoblast cells in the junction layer and near the decidua layer on the scarred side were higher than those of the control on day 15.5 (31.01±1.502 vs. 23.63±0.90, t=12.76, P<0.001) and day 17.5 (31.96±2.37 vs. 24.03±1.87, t=4.36, P=0.008), respectively. In the mature placenta on the scarred side on day 18.5, CK7+ traced trophoblast cells were abundant in the decidua layer near the maternal side, showing an overall excessive trophoblast invasion. Conclusion:Scarred uterus in mice affects the endometrial function, contributing to reduced endometrial receptivity during pregnancy and excessive invasion of trophoblasts during placental development after implantation.