Objective To study the mechanism underlying intrauterine adhesion fibrosis and the origin of fibroblasts in the repair of endometrial fibrosis. Design An experimental study involving an animal model of intrauterine adhesion and detection of fibrosis-related molecules. Setting Institute of Reproductive Health, Tongji Medical College. Population or Sample Forty-five adult (8-week-old) female Sprague–Dawley rats. Methods The levels of molecular factors related to the endothelial-to-mesenchymal transition (EndMT) were examined in a rat model of intrauterine adhesion using immunofluorescence, immunohistochemistry, qPCR and Western blot analyses. Main Outcome Measures Levels of the endothelial marker CD31 and the mesenchymal markers alpha-smooth muscle actin (α-SMA) and vimentin. Results Decreased CD31 levels and increased α-SMA and vimentin levels indicate that EndMT is involved in intrauterine adhesion fibrosis. Conclusions Endothelial cells promote the emergence of fibroblasts via the EndMT during the endometrial fibrosis of intrauterine adhesions. Funding This study was funded by National Natural Science Foundation of China (81971435). Keywords Intrauterine adhesion，EndMT, fibrosis