卵巢纤维化是卵巢子宫内膜异位囊肿影响卵巢功能的最显著特征，表现为卵巢正常组织减少、窦卵泡数下降和卵巢血供减少。然而关于卵巢纤维化的发生远未被认知，其形成机制也不明确。我们前期研究发现共培养子宫内膜间充质干细胞与子宫内膜间质细胞后，间质细胞增殖能力增强、VEGF及β-catenin表达上调，并且在深部内异病灶中已发现存在异位子宫内膜间质细胞向肌成纤维细胞转化的现象，提示在卵巢子宫内膜异位囊肿所致卵巢纤维化中亦可能存在异位子宫内膜间质细胞的异常增殖及转化，而间充质干细胞在异位间质细胞的异常生物学行为中具有重要作用，但其具体作用机制尚不清楚。基于以上基础及问题，本项目首次以影响卵巢储备功能的根本原因- - 卵巢纤维化为研究点，从在体与细胞及分子水平阐明卵巢子宫内膜异位囊肿所致卵巢纤维化的机制，明确间充质干细胞在纤维化发生发展中的作用，为正确治疗卵巢子宫内膜异位囊肿并阻止卵巢纤维化进程提供理论指导。

Ovarian endometrotic cysts may impair ovarian function, result in the feature of fibrosis, present as declined ovarian normal tissue, reduced antral follicle count and decreased ovarian blood supply, but the mechanism is poorly understood. Our previous studies have found that endometrial stromal cell proliferation is enhanced when co-cultured with endometrial mesenchymal stem cells, with up-regulation in the expression of VEGF and β-catenin. Meanwhile, the potential of endometriotic stromal cells in transformation to myofibroblast has also been noticed. However, the definite transformation mechanism and the role of mesenchymal stem cells played in the process still remains unknown. Based on the effect of ovarian fibrosis on ovarian function injury, we will determine the role of mesenchymal stem cells in the process of fibrosis, illustrate the cellular and molecular mechanism . This study will provide a theoretical support for the treatment of ovarian endometrotic cysts and prevention of ovarian fibrosis.