Progress of Research on the Pathogenesis of Endometriosis

蓉蓉 赵
In: Journal of Clinical Personalized Medicine · 2025 · vol. 04(03) , pp. 84–92 · doi:10.12677/jcpm.2025.43319 · W4410866479
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⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

Endometriosis pathogenesis involves ectopic endometrial survival, invasion, immune dysregulation, stem cell migration, endocrine imbalance, epigenetic changes, microRNA activity, gut microbiota, ferroptosis, and environmental factors.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-06 ⓘ

This paper is a 2025 narrative review of current research on endometriosis pathogenesis, synthesizing proposed mechanisms across retrograde and metastatic dissemination, coelomic metaplasia/embryonic rest, immune microenvironment dysregulation, stem-cell recruitment (including endometrial and bone marrow sources), endocrine and epigenetic regulation, and emerging roles for microRNAs, intestinal dysbiosis, iron-dependent cell death (ferroptosis), and environmental exposures. It emphasizes that immune cell abnormalities (neutrophils, macrophages, NK cells, and mast cells) interact with inflammation, angiogenesis, and neural sensitization, while endocrine imbalance and epigenetic changes jointly promote lesion proliferation and implantation; microRNAs (e.g., via PTEN-related angiogenesis control) and ferroptosis are highlighted as additional molecular pathways. The review explicitly cautions that no single theory fully explains all forms and that causal links—especially for gut microbiome changes—remain insufficiently established. This paper is centrally about endometriosis — it provides a broad update on the field’s proposed mechanisms of endometriosis pathogenesis and progression, with multiple sections describing how these interact.

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Abstract

子宫内膜异位症(Endometriosis, EMS)是一种以子宫内膜组织异位生长为特征的复杂疾病，其机制涉及异位内膜的存活、侵袭及免疫微环境失衡。经典理论(经血逆流、良性转移)难以解释腹膜外病灶，而体腔化生及胚胎休止理论则从苗勒管发育异常角度提供补充。近年研究聚焦于免疫微环境失调，中性粒细胞、巨噬细胞及NK细胞功能异常通过炎症反应、血管生成及神经敏化促进疾病进展；干细胞理论指出子宫内膜或骨髓来源的干细胞经逆流或循环系统迁移至异位部位，分化为病变组织，为深部及腹膜外病灶提供新解释。内分泌失衡与表观遗传调控协同驱动异位内膜增殖。MicroRNAs通过靶向PTEN等基因调节血管生成，而肠道菌群失调可能经免疫及雌激素轴加剧病理进程。铁死亡在清除异位细胞与诱导纤维化间呈现双向作用，环境因素(二噁英、生活方式)亦参与调控。EMS的发病机制呈现出多因素交互的病理网络，未来需整合分子机制与临床转化，继续探索新型病理生理机制及治疗策略。Endometriosis (EMS) is a complex disease characterized by ectopic growth of endometrial tissue, and its mechanism involves survival, invasion and imbalance of the immune microenvironment of the ectopic endometrium. Classical theories (retrograde menstrual flow, benign metastasis) are difficult to explain the extraperitoneal foci, while somatic chemotaxis and embryonic resting theories provide complementary perspectives in terms of abnormal mullerian duct development. Recent studies have focused on dysregulation of the immune microenvironment, with abnormalities in neutrophil, macrophage, and NK cell function contributing to disease progression through inflammatory responses, angiogenesis, and neural sensitization. Stem cell theory suggests that endometrial or bone marrow-derived stem cells migrate via the retrograde flow or circulatory system to ectopic sites, where they can differentiate into diseased tissues, providing new explanations for deep and extraperitoneal lesions. Endocrine imbalance and epigenetic regulation synergistically drive ectopic endothelial proliferation. microRNAs regulate angiogenesis by targeting genes such as PTEN, and intestinal dysbiosis may exacerbate the pathologic process via the immune and estrogenic axes. The pathogenesis of EMS is characterized by a multifactorial pathological network, and the integration of molecular mechanisms and clinical translation is needed to explore novel pathophysiological mechanisms and therapeutic strategies.

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endometriosis

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