Endometrial Anomalies in Women with Endometriosis

Kathy L. Sharpe-Timms, K L Sharpe-Timms
Annals of the New York Academy of Sciences · 2001 · vol. 943(1) , pp. 131–147 · doi:10.1111/j.1749-6632.2001.tb03797.x · PMID:11594534 · W2017793326
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Eutopic endometrium from women with endometriosis exhibits structural, immunological, and molecular anomalies compared to endometrium from women without the condition.

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Abstract

Endometriotic lesions are defined by extrauterine growth of endometrial glands and stroma. Retrograde menstruation with subsequent attachment, invasion, and neovascularization are believed to give rise to the endometriotic lesions. As most women exhibit some degree of retrograde menstruation, some other unidentified factor(s) must render certain women susceptible to attachment and growth of ectopic endometrial tissue. A variety of theories have been proposed to account for this susceptibility, including genetic predisposition, aberrant immunological response, and an altered peritoneal environment. Ectopic endometriotic lesions are histologically similar to their putative eutopic precursors, yet significant biochemical differences exist between these two tissues. Less information is available regarding differences between eutopic endometrium from women with or without endometriosis. This report describes anomalies in structure, proliferation, immune components, adhesion molecules, proteolytic enzymes and inhibitors, steroid and cytokine production and responsiveness, and gene expression and protein production that have been identified in eutopic endometrium from women with endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium Apoptosis Apoptosis Cell Division Cell Division Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Gene Expression Regulation Gene Expression Regulation Humans Protein Biosynthesis

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 (88)

Cited by (50)

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