Apoptosis and endometriosis

Tasuku Harada, Fuminori Taniguchi, Masao Izawa, Yoko Ohama, Yasuko Takenaka, Yukiko Tagashira, Ayako Ikeda, Ayako Watanabe, Tomio Iwabe, Naoki Terakawa
Frontiers in bioscience : a journal and virtual library · 2007 · vol. 12(8-12) , pp. 3140 · doi:10.2741/2302 · PMID:17485289 · W4296992478
article OA: bronze CC0 ⤵ 53 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

This review examines the role of apoptosis in normal endometrium and its altered regulation in eutopic and ectopic endometrial tissues from women with endometriosis, as well as its therapeutic implications.

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, 2026-06-10 ⓘ

This paper is a current literature review examining the physiological role of apoptosis in normal uterine endometrium and the altered regulation of apoptosis in eutopic and ectopic endometrial tissue from women with endometriosis. It summarizes evidence that apoptosis contributes to endometrial tissue homeostasis during the menstrual cycle by eliminating senescent cells, and discusses apoptosis-related systems such as BCL-2 family and Fas/FasL that have been studied in both human endometrium and endometriotic tissues. A key focus is reported apoptosis activity in eutopic and ectopic endometrium in endometriosis and how differences in eutopic endometrium may support survival of regurgitated cells. As a narrative review, it does not provide new experimental data or a stated quantitative limitation beyond its scope in linking apoptosis biology and potential therapeutic roles. This paper is centrally about endometriosis — it reviews apoptosis mechanisms in eutopic and ectopic endometrial tissues and connects them to endometriosis biology and treatment discussion.

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

Abstract

Apoptosis plays a critical role in maintaining tissue homeostasis and represents a normal function to eliminate excess or dysfunctional cells. Accumulated evidence suggest that apoptosis helps to maintain cellular homeostasis during the menstrual cycle by eliminating senescent cells from the functional layer of the uterine endometrium during the late secretory and menstrual phase of the cycle. BCL-2 family and Fas/FasL system have been extensively studied in human endometrium and endometriotic tissues. Eutopic endometrium from women with endometriosis reportedly has some fundamental differences compared with normal endometrium of women without endometriosis. The differences could contribute to the survival of regurgitating endometrial cells into the peritoneal cavity and the development of endometriosis. One mechanism that recently gained a lot of interest is the finding that apoptosis appeared in eutopic and ectopic endometrium of patients with endometriosis. This study is a current review of the literature focused on the physiological role of apoptosis in normal endometrium and the alterations in regulation of apoptosis in eutopic and ectopic endometrium from women with endometriosis. Finally, role of apoptosis in the treatment of endometriosis is reviewed to link the basic research findings into clinical applications.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Apoptosis Apoptosis Apoptosis Endometriosis Endometriosis Endometrium Endometrium Female Humans

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 (87)

Cited by (50)

Source provenance

europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:15:00.519696+00:00
License: CC0 · commercial use OK