Kirkwood Phoebe M, Shaw Isaac W, Saunders Philippa T K
Centre for Inflammation Research, The University of Edinburgh, Edinburgh, United Kingdom.
Front Reprod Health. 2022 Jan 6;3:801843. doi: 10.3389/frph.2021.801843. eCollection 2021.
The human endometrium is a remarkable tissue which may experience up to 400 cycles of hormone-driven proliferation, differentiation and breakdown during a woman's reproductive lifetime. During menstruation, when the luminal portion of tissue breaks down, it resembles a bloody wound with piecemeal shedding, exposure of underlying stroma and a strong inflammatory reaction. In the absence of pathology within a few days the integrity of the tissue is restored without formation of a scar and the endometrium is able to respond appropriately to subsequent endocrine signals in preparation for establishment of pregnancy if fertilization occurs. Understanding mechanisms regulating scarless repair of the endometrium is important both for design of therapies which can treat conditions where this is aberrant (heavy menstrual bleeding, fibroids, endometriosis, Asherman's syndrome) as well as to provide new information that might allow us to reduce fibrosis and scar formation in other tissues. Menstruation only occurs naturally in species that exhibit spontaneous stromal cell decidualization during the fertile cycle such as primates (including women) and the Spiny mouse. To take advantage of genetic models and detailed time course analysis, mouse models of endometrial shedding/repair involving hormonal manipulation, artificial induction of decidualization and hormone withdrawal have been developed and refined. These models are useful in modeling dynamic changes across the time course of repair and have recapitulated key features of endometrial repair in women including local hypoxia and immune cell recruitment. In this review we will consider the evidence that scarless repair of endometrial tissue involves changes in stromal cell function including mesenchyme to epithelial transition, epithelial cell proliferation and multiple populations of immune cells. Processes contributing to endometrial fibrosis (Asherman's syndrome) as well as scarless repair of other tissues including skin and oral mucosa are compared to that of menstrual repair.
人类子宫内膜是一种非凡的组织,在女性的生殖寿命期间,它可能经历多达400个由激素驱动的增殖、分化和分解周期。在月经期间,当组织的腔内部分分解时,它类似于一个有碎片脱落的血性伤口,下层基质暴露并伴有强烈的炎症反应。在没有病理学问题的情况下,几天内组织的完整性即可恢复,不会形成疤痕,并且如果受精发生,子宫内膜能够对随后的内分泌信号做出适当反应,为怀孕做准备。了解调节子宫内膜无瘢痕修复的机制,对于设计能够治疗这种异常情况(月经过多、子宫肌瘤、子宫内膜异位症、阿谢曼综合征)的疗法很重要,同时也能提供新的信息,使我们有可能减少其他组织中的纤维化和瘢痕形成。月经仅自然发生于在生育周期中表现出自发性基质细胞蜕膜化的物种,如灵长类动物(包括人类)和刺毛鼠。为了利用遗传模型和详细的时间进程分析,已经开发并完善了涉及激素操纵、人工诱导蜕膜化和激素撤退的子宫内膜脱落/修复小鼠模型。这些模型有助于模拟修复过程中的动态变化,并重现了女性子宫内膜修复的关键特征,包括局部缺氧和免疫细胞募集。在这篇综述中,我们将考虑证据表明子宫内膜组织的无瘢痕修复涉及基质细胞功能的变化,包括间充质向上皮转化、上皮细胞增殖和多种免疫细胞群体。将导致子宫内膜纤维化(阿谢曼综合征)的过程以及包括皮肤和口腔黏膜在内的其他组织的无瘢痕修复过程与月经修复过程进行比较。