细胞自噬通过调控上皮间质转化影响宫腔粘连的研究
摘要
宫内膜纤维化及上皮-间质转化(Epithelial-Mesenchymal Transition,EMT)。细胞自噬(Autophagy)在组织纤维化
进程中的关键调控作用,本研究旨在阐明自噬在IUA发生发展中的病理学意义及其对EMT的调控机制。本研究分别
构建大鼠IUA体内模型及TGF-β诱导的子宫内膜上皮细胞体外模型,并给予自噬激动剂雷帕霉素(Rapamycin)进
行干预。结果表明,IUA模型组中细胞自噬水平显著抑制,并伴随氧化应激加剧、炎症因子过度释放以及E-cadherin
表达下调,Vimentin表达上调的EMT表型改变。经雷帕霉素干预后,自噬相关标志物表达显著上调,抑制p62累积。
干预组EMT进程被有效逆转,羟脯氨酸(HYP)含量及活性氧(ROS)水平显著降低,内膜胶原沉积明显改善。综
上所述,自噬功能受损是驱动IUA内膜纤维化进展的关键因素,靶向激活细胞自噬可有效拮抗子宫内膜EMT进程,
为IUA的临床防治提供了潜在的治疗靶点与理论依据。
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