Apoptosis and the Pathogenesis of Endometriosis

Juan A Garcia-Velasco, Juan A. García-Velasco, Aydin Arici, Aydın Arıcı
Seminars in reproductive medicine · 2003 · vol. 21(2) , pp. 165–172 · doi:10.1055/s-2003-41323 · PMID:12917786 · W2403788804
review OA: closed CC0 ⤵ 45 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review summarizes research on apoptosis, highlighting how its decreased regulation and increased survival of endometriotic cells, influenced by sex steroids and cell adhesion, contribute to endometriosis pathogenesis.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

This paper reviews apoptosis as a mechanism for deleting unwanted cells without triggering inflammation, focusing on evidence that endometriotic implants survive by resisting apoptosis and existing in an inflammatory environment. It summarizes findings from studies of eutopic endometrial cells in women with endometriosis that show further resistance to apoptosis compared with disease-free controls, and it reviews apoptosis-related pathways including bcl-2/bax and fas/fas ligand, emphasizing how sex steroids and cell adhesion regulation may modulate early events. The paper is explicitly a narrative review that compiles prior literature rather than presenting new experiments, and it does not provide a unified mechanistic conclusion. This paper is centrally about endometriosis — it focuses on apoptosis pathways (bcl-2/bax and fas/fas ligand) and related sex-steroid and adhesion regulation in endometriosis pathogenesis.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Apoptosis is a physiologic process that deletes unwanted cells without inducing an inflammatory reaction. Survival of endometriotic implants is associated with decreased apoptosis and an inflammatory environment. The most widely accepted theory-transplantation theory-related to the pathogenesis of endometriosis is supported by the description of abnormal survival of regurgitated endometrial cells. Eutopic endometrial cells from women with endometriosis also seem to resist apoptosis further when compared with cells from disease-free women. Several apoptotic pathways have been studied. Recent literature concerning apoptosis-related genes such as bcl-2/bax and fas/fas ligand is summarized in this article. Special emphasis is placed on sex steroid modulation and cell adhesion regulation, both relevant in early events of endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Apoptosis Endometriosis Cell Adhesion Endometriosis Endometriosis Endometriosis Fas Ligand Protein fas Receptor fas Receptor Female Humans Immunity Membrane Glycoproteins Membrane Glycoproteins Proto-Oncogene Proteins c-bcl-2 Proto-Oncogene Proteins c-bcl-2

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.

Cited by (45)

Source provenance

europepmc
last seen: 2026-06-16T06:07:01.518242+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:12:50.257867+00:00
unpaywall
last seen: 2026-06-02T02:00:03.124865+00:00
License: CC0 · commercial use OK