Molecular and Cellular Changes in the Pathogenesis of Endometriosis

Konstantin A. Toniyan, О. И. Орлов, V. V. Boyarintsev, Irina V. Ogneva
In: Human Physiology · 2021 · vol. 47(6) , pp. 690–699 · doi:10.1134/s0362119721060116 · W4200548694
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review explores molecular and cellular alterations in endometriosis pathogenesis, including immune responses, hormonal changes, steroid receptor activity, and epithelial-mesenchymal transition in endometrial cells.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This paper is a narrative review of molecular and cellular alterations implicated in endometriosis pathogenesis, focusing on evidence related to innate and adaptive immunity, disruptions in hormonal status and steroid hormone nuclear receptors, and a potential epithelial–mesenchymal transition (EMT) in endometrial cells involved in ectopic lesion establishment. It synthesizes literature suggesting that multiple interacting factors—including immune dysregulation, hormone-dependent signaling, and phenotypic changes in endometrial cells—may jointly drive ectopic focus formation. A key limitation is that the work is based on curated literature summaries rather than presenting new experimental data. This paper is centrally about endometriosis — it reviews molecular and cellular mechanisms such as immune changes, steroid receptor alterations, and EMT in ectopic lesion development.

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Abstract

The review examines molecular and cell changes in the pathogenesis of endometriosis. Literature data on innate and adaptative immunity are presented, the role of changes in the hormonal status and nuclear receptors for steroid hormones is considered, and a possible epithelial–mesenchymal transition in endometrial cells and at the site of their attachment during the formation of an ectopic focus of endometrium is discussed. The role of the combined action of various factors in the pathogenesis of endometriosis is discussed.

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Condition tags

endometriosis

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.

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