AimEndometriosis is a complex, multifactorial disease. Recent advances in molecular biology underscore that somatic mutations within the epithelial component of the normal endometrium, alongside aberrant epigenetic alterations within endometrial stromal cells, may serve as stimulators for the proliferation of endometriotic tissue within the peritoneal cavity. Nevertheless, pivotal inquiries persist: the deterministic factors driving endometriosis development in certain women while sparing others, notwithstanding comparable experiences of retrograde menstruation. Within this review, we endeavor to synopsize the current understanding of diverse pathophysiologic mechanisms underlying the initiation and progression of endometriosis and delineate avenues for future research.MethodsA literature search without time restriction was conducted utilizing PubMed and Google Scholar.ResultsGiven that aberrant clonal expansion stemming from cancer‐associated mutations is common in normal endometrial tissue, only endometrial cells harboring mutations imparting proliferative advantages may be selected for survival outside the uterus. Endometriotic cells capable of engendering metabolic plasticity and modulating mitochondrial dynamics, thereby orchestrating responses to hypoxia, oxidative stress, inflammation, hormonal stimuli, and immune surveillance, and adeptly acclimating to their harsh surroundings, stand a chance at viability.ConclusionThe genesis of endometriosis appears to reflect the evolutionary principles of mutation, selection, clonal expansion, and adaptation to the environment.

中文翻译：

---

重新思考子宫内膜异位症的发病机制：基因组、表观遗传和环境因素的复杂相互作用


目的子宫内膜异位症是一种复杂的、多因素的疾病。分子生物学的最新进展强调，正常子宫内膜上皮成分内的体细胞突变，以及子宫内膜基质细胞内的异常表观遗传改变，可能会刺激腹膜腔内子宫内膜异位组织的增殖。尽管如此，关键的问题仍然存在：尽管存在类似的逆行月经经历，但决定性因素推动某些女性发生子宫内膜异位症，而另一些女性则不受此影响。在这篇综述中，我们努力概述目前对子宫内膜异位症发生和进展的不同病理生理机制的理解，并为未来的研究描绘出途径。方法利用 PubMed 和 Google Scholar 进行无时间限制的文献检索。结果鉴于异常克隆扩增源于癌症相关突变在正常子宫内膜组织中很常见，只有携带具有增殖优势的突变的子宫内膜细胞才可能被选择在子宫外生存。子宫内膜异位细胞能够产生代谢可塑性并调节线粒体动力学，从而协调对缺氧、氧化应激、炎症、激素刺激和免疫监视的反应，并熟练地适应恶劣的环境，有机会获得生存能力。结论子宫内膜异位症的起源似乎是反映了突变、选择、克隆扩张和适应环境的进化原理。