The Origin and Pathogenesis of Endometriosis

review OA: bronze CC0 ⤵ 331 in-corpus citations
AI-generated summary by claude@2026-06, 2026-06-07

This review outlines a model where aberrant progenitor cells from the endometrium implant outside the uterus, forming lesions that recruit stromal cells, undergo inflammation driven by NF-κB and steroid hormone receptor pathways, and acquire cancer-associated mutations.

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Abstract

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.

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Condition tags

endometriosisdie_deep_infiltrating

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Estrogen Receptor beta Estrogen Receptor beta Estrogen Receptor beta Female Humans Menstruation Menstruation Ovarian Neoplasms Ovarian Neoplasms Ovarian Neoplasms Receptors, Progesterone Receptors, Progesterone Receptors, Progesterone Signal Transduction

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (50)

Source provenance

europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:22:35.348889+00:00
License: CC0 · commercial use OK