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子宫内膜异位症(EMs)是育龄期妇女常见的一种多基因、多因素发病的良性疾病,但是目前具体发病机制尚不明确。最近研究表明PGE2与EMs的发病及相关并发症的发生密切相关。EMs具有雌激素依赖性,患者体内机体免疫细胞清除机制受到抑制,其体内PGE2水平升高,不但可以直接促进异位内膜细胞的存活和增殖,而且具有促进雌激素合成、抑制机体免疫细胞清除机制及促进生长因子产生的作用。因此,PGE2通过直接与间接途径对EMs中异位内膜的存活和增殖进行调节,对EMs的发病具有重要作用。但是目前还不能表明PGE2对EMs作用的确切病理机制,尚需进一步研究明确PGE2信号通路异常的分子机制。
Endometriosis (EMs) is a common polygenic and multifactorial benign disease in women of childbearing age, but the specific pathogenesis is not yet clear. Recent studies have shown that PGE2 and EMs incidence and related complications are closely related. EMs is estrogen-dependent, and the mechanism of immune cell clearance is inhibited in vivo. The elevated level of PGE2 in vivo can not only directly promote the survival and proliferation of ectopic endometrial cells, but also promote the synthesis of estrogen and inhibit the clearance of immune cells Mechanism and promote the role of growth factors. Therefore, PGE2 regulates the survival and proliferation of ectopic endometrium in EMs through direct and indirect pathways, which plays an important role in the pathogenesis of EMs. However, the exact pathological mechanism of the effect of PGE2 on EMs can not be demonstrated at present, and further studies on the molecular mechanism of the abnormal PGE2 signaling pathway are needed.