Endometriosis is a common chronic inflammatory condition in which endometrial tissue appears outside the uterine cavity. Because ectopic endometriosis cells express both estrogen and progesterone (P4) receptors, they grow and undergo cyclic proliferation and breakdown similar to the endometrium. This debilitating gynecological disease affects up to 15% of reproductive aged women. Despite many years of research, the etiopathogenesis of endometrial lesions remains unclear. Retrograde transport of the viable menstrual endometrial cells with retained ability for attachment within the pelvic cavity, proliferation, differentiation and subsequent invasion into the surrounding tissue constitutes the rationale for widely accepted implantation theory. Accordingly, the most abundant cells in the endometrium are endometrial stromal cells (EnSCs). These cells constitute a particular population with clonogenic activity that resembles properties of mesenchymal stem/stromal cells (MSCs). Thus, a significant role of stem cell-based dysfunction in formation of the initial endometrial lesions is suspected. There is increasing evidence that the role of epigenetic mechanisms and processes in endometriosis have been underestimated. The importance of excess estrogen exposure and P4 resistance in epigenetic homeostasis failure in the endometrial/endometriotic tissue are crucial. Epigenetic alterations regarding transcription factors of estrogen and P4 signaling pathways in MSCs are robust in endometriotic tissue. Thus, perspectives for the future may include MSCs and EnSCs as the targets of epigenetic therapies in the prevention and treatment of endometriosis. Here, we reviewed the current known changes in the epigenetic background of EnSCs and MSCs due to estrogen/P4 imbalances in the context of etiopathogenesis of endometriosis.

子宫内膜异位症是一种常见的慢性炎症，子宫内膜组织出现在子宫腔外。由于异位子宫内膜异位细胞同时表达雌激素和孕激素 (P4) 受体，因此它们会像子宫内膜一样生长并经历周期性增殖和分解。这种使人衰弱的妇科疾病影响高达 15% 的育龄妇女。尽管经过多年的研究，子宫内膜病变的发病机制仍不清楚。存活的月经子宫内膜细胞的逆行运输，保留在盆腔内附着、增殖、分化和随后侵入周围组织的能力，构成了广泛接受的着床理论的基本原理。因此，子宫内膜中最丰富的细胞是子宫内膜基质细胞（EnSC）。这些细胞构成了具有克隆形成活性的特定群体，类似于间充质干细胞/基质细胞（MSC）的特性。因此，怀疑基于干细胞的功能障碍在初始子宫内膜病变的形成中发挥重要作用。越来越多的证据表明，表观遗传机制和过程在子宫内膜异位症中的作用被低估了。过量雌激素暴露和 P4 抵抗在子宫内膜/子宫内膜异位组织表观遗传稳态失败中的重要性至关重要。间充质干细胞中雌激素转录因子和 P4 信号通路的表观遗传改变在子宫内膜异位组织中是强烈的。因此，未来的前景可能包括将 MSC 和 EnSC 作为表观遗传疗法预防和治疗子宫内膜异位症的靶标。在此，我们回顾了子宫内膜异位症发病机制中雌激素/P4 失衡导致的 EnSC 和 MSC 的表观遗传背景目前已知的变化。