Apoptosis in Endometriosis

Admir Agic, Schima Djalali, Klaus Diedrich, Daniela Hornung
Gynecologic and obstetric investigation · 2009 · vol. 68(4) , pp. 217–223 · doi:10.1159/000235871 · PMID:19729941 · W2078095427
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review outlines the molecular basis of apoptosis and summarizes literature on altered apoptosis regulation in eutopic and ectopic endometrium from women with endometriosis.

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Abstract

Apoptosis is a physiologic process that eradicates undesired cells without inducing an inflammatory reaction. It is an important regulator of eutopic endometrial function and evidence suggests that apoptosis aids in maintaining cellular homeostasis during the menstrual cycle by eliminating aging cells from the functional layer of the uterine endometrium. Endometriosis, which is characterized by the growth of endometrial tissue outside the uterus, could result from increased cellular proliferation or decreased apoptosis in response to appropriate stimuli. Eutopic endometrium from women with endometriosis has several differences compared with normal endometrium of women without endometriosis. These differences may contribute to the survival of regurgitated endometrial cells into the peritoneal cavity and thus to the development of endometriosis. In this article, we will summarize recent literature concerning apoptosis-related genes such as Bcl-2 and Fas, outline the molecular basis of apoptosis and review the literature focused on the alterations in regulation of apoptosis in eutopic and ectopic endometrium from women with endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Apoptosis Apoptosis Apoptosis Endometriosis Caspases Caspases Caspases Endometriosis Endometriosis Endometrium Endometrium Endometrium Epithelium Epithelium Fas Ligand Protein Fas Ligand Protein Fas Ligand Protein fas Receptor fas Receptor fas Receptor

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 (50)

Cited by (50)

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