Endometriosis: Cell Death and Cell Signaling Machinery

Ginearosa Carbone, Katherine Nelson, Claire Baumgartner, Ann M Bode, Akimasa Takahashi, Ilana Chefetz
Endocrinology · 2023 · vol. 164(6) · doi:10.1210/endocr/bqad057 · PMID:37216932 · W4377290326
review OA: bronze CC0 ⤵ 7 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review examines the pathologic processes of endometriosis, focusing on cell signaling and cell death pathways, stem cells, and treatment regimens for this gynecologic disorder.

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Abstract

Endometriosis is an estrogen-dependent disorder defined as the deposition and growth of endometrial tissue outside the uterus, including but not limited to the pelvic peritoneum, rectovaginal septum, and ovaries. Endometriosis is a substantial contributor to pelvic pain and subfertility and has been associated with an increased incidence of certain cancers, including ovarian. Appropriate treatment of endometriosis can reduce morbidity, but generally is used only to address symptoms, since no cure currently exists. Multifactorial etiologies for endometriosis have been proposed, with significant evidence for genetic, immune, and environmental causes. Recent advances suggest that molecular signaling and programmed cell death pathways are involved in endometriosis, suggesting avenues for future curative treatments. The goal of this review is to examine the pathologic processes of endometriosis, focusing on cell signaling and cell death pathways, stem cells, treatment regimens, and future directions surrounding this gynecologic disorder.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Cell Death Cell Death Cell Death Cell Death Cell Death

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 (71)

Cited by (7)

Source provenance

europepmc
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License: CC0 · commercial use OK