Recent molecular genetic findings on endometriosis and normal endometrium suggest a modified model in which circulating epithelial progenitor or stem cells intended to regenerate uterine endometrium after menstruation may become overreactive and trapped outside the uterus. These trapped epithelium-committed progenitor cells form nascent glands through clonal expansion and recruit polyclonal stromal cells, leading to the establishment of deep infiltrating endometriosis. Once formed, the ectopic tissue becomes subject to immune surveillance, resulting in chronic inflammation. The inflammatory response orchestrated by nuclear factor-κB signaling is exacerbated by aberrations in the estrogen receptor-β and progesterone receptor pathways, which are also affected by local inflammation, forming a dysregulated inflammation-hormonal loop. Glandular epithelium within endometriotic tissue harbors cancer-associated mutations that are frequently detected in endometriosis-related ovarian cancers. In this review, we summarize recent advances that have illuminated the origin and pathogenesis of endometriosis and have provided new avenues for research that promise to improve the early diagnosis and management of endometriosis.

中文翻译：

---

子宫内膜异位症的起源和发病机制。

最近关于子宫内膜异位症和正常子宫内膜的分子遗传学发现提示了一种改良的模型，在这种模型中，意欲在月经后再生子宫内膜的循环上皮祖细胞或干细胞可能过度反应并被困在子宫外。这些捕获的上皮成分祖细胞通过克隆扩增形成新生腺体并募集多克隆基质细胞，从而导致深层浸润性子宫内膜异位症的建立。一旦形成，异位组织将受到免疫监视，从而导致慢性炎症。核因子-κB信号所策划的炎症反应会因雌激素受体-β和孕激素受体途径的异常而加剧，它们也受到局部炎症的影响，形成失调的炎症-激素循环。子宫内膜异位组织内的腺上皮具有与癌症相关的突变，在子宫内膜异位相关的卵巢癌中经常发现这种突变。在这篇综述中，我们总结了最近的进展，这些进展阐明了子宫内膜异位症的起源和发病机理，并为有望改善子宫内膜异位症的早期诊断和管理提供了新的研究途径。