宫腔粘连（IUA）是子宫内膜基底层损伤后以内膜纤维化为特征的疾病，是子宫性不孕的重要原因。目前缺乏有效治疗方法。我们前期研究发现调控上皮-间质转化（EMT）的重要分子ΔNp63在IUA残存内膜上皮细胞显著高表达，并促进内膜纤维化。体外实验证明，高表达ΔNp63的子宫内膜上皮细胞增殖及分化被抑制，并有向肌成纤维细胞分化倾向。用诱导纤维化药物刺激子宫内膜上皮细胞，诱导出ΔNp63高表达，且上皮表型向成纤维细胞转化。相反，碱性成纤维细胞生长因子（bFGF）可通过抑制ΔNp63表达，恢复上皮自身增殖能力，逆转EMT过程，遏制纤维化。我们的科学假说是：①子宫内膜损伤诱导残存内膜上皮重编程，使其高表达ΔNp63；②异源性高表达ΔNp63的子宫内膜上皮不能增殖并分化成内膜上皮细胞，而是向肌成纤维细胞转分化；③bFGF可逆转宫腔粘连时以ΔNp63为中心的异常分子信号转导机制，从而促进功能性子宫内膜再生。

Intrauterine adhesions (IUA) are a disease characterized by endometrial fibrosis after injury of endometrial basal layer. IUA is an important cause of uterine associated infertility and there is no effective treatment for it. Our previous study found that ΔNp63, an important molecular for regulation of epithelial mesenchymal transition (EMT) was significantly increased in residual endometrial epithelial cells from patients with IUA and promoted the endometrial fibrosis. In vitro experiments showed that ΔNp63-expressed human endometrial epithelial cells showed inhibition of proliferation and differentiation and a tendency of differentiation into myofibroblast. Additionally, using fibrosis inducing drug to treat primary endometrial epithelial cells, the cells showed high expression of ΔNp63 along with phenotype switch from epithelium to myofibroblast. On the contrary, basic fibroblast growth factor (bFGF) recovered the proliferation of epithelial cells, reversed the EMT process and suppressed the fibrosis by inhibiting the expression of ΔNp63. Our scientific hypotheses are: (1) endometrial damage induces the residual endometrial epithelial reprogramming, promoting the expression of ΔNp63; (2) high expression of ΔNp63 blocks the proliferation and differentiation of endometrial epithelium into endometrial epithelial cells, but into myofibroblast; (3) bFGF could reverse the abnormal signal transduction in which ΔNp63 as the central molecular in IUA, promoting the functional endometrial regeneration.