A possible Molecular Mechanism of Adenomyosis

Guoyun Wang
In: Journal of Gynecology and Womens Health · 2017 · vol. 4(3) · doi:10.19080/jgwh.2017.04.555637 · W2768159597
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⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

This paper investigates a potential molecular mechanism underlying adenomyosis.

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

This mini review discusses proposed molecular mechanisms underlying adenomyosis, an estrogen-dependent inflammatory disease characterized by endometrial glands and stroma deep in the myometrium, focusing on how endometrium invaginates into the myometrium and what might drive that process. It synthesizes evidence that epithelial-mesenchymal transition (EMT) is involved in adenomyosis and endometriosis lesions and notes macrophage involvement, including reports of increased stromal macrophage populations in adenomyosis and decreased CD68-positive macrophage infiltration after GnRH agonist treatment, while acknowledging that the definite mechanism of macrophage-driven adenomyosis remains vague. The author presumes that macrophages may induce endometrial epithelial cells to undergo EMT, drawing on macrophage-induced EMT findings from other diseases such as tissue remodeling and tumor progression, and frames this as a possible mechanism by which misplaced endometrial cells could contribute to disease development. Relevance to endometriosis: the paper explicitly contrasts adenomyosis and endometriosis by tissue site and cites EMT being crucial in both adenomyosis and endometriosis lesions, though its main focus is proposing a macrophage-induced EMT mechanism in adenomyosis.

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Abstract

Journal of Gynecology and Women’s Health is a peer-reviewed, multidisciplinary, international journal of Juniper group that publishes scientific works within the field of obstetrics, gynecology and women’s health.

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Condition tags

adenomyosis

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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last seen: 2026-06-10T17:14:06.276822+00:00
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