Involvement of resistance to apoptosis in the pathogenesis of endometriosis.

Kaei Nasu, K Nasu, A Yuge, Akitoshi Yuge, A Tsuno, M Nishida, Masakazu Nishida, Hisashi Narahara, H Narahara
Histology and histopathology · 2009 · vol. 24(9) , pp. 1181–92 · doi:10.14670/hh-24.1181 · PMID:19609865 · W2166154664
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review examines how altered expression of apoptosis-related molecules contributes to the survival and ectopic growth of endometrial cells in endometriosis.

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

This paper reviews evidence on how altered apoptosis regulates endometrial cells in endometriosis, comparing normal endometrium from women without disease to eutopic and ectopic endometrium from women with endometriosis. It reports that endometriosis is associated with dysregulated proliferative and apoptotic control, where decreased apoptosis helps ectopic endometrial cells survive and implant, and where this is linked to higher expression of anti-apoptotic factors and lower expression of pro-apoptotic factors, including impaired transmission of a “death” signal. The paper also discusses ongoing basic and clinical research on medical treatments for endometriosis through the lens of apoptosis, while noting its scope as a literature review rather than original experimental work. This paper is centrally about endometriosis — it focuses on resistance to apoptosis and apoptosis-associated molecule expression in the pathogenesis of endometriosis.

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Abstract

Endometriosis, a disease affecting 3-10% of women of reproductive age, is characterized by the ectopic growth of endometrial tissue. Increasingly, endometriosis is also becoming recognized as a condition in which ectopic endometrial cells exhibit abnormal proliferative and apoptotic regulation in response to appropriate stimuli. Apoptosis plays a critical role in maintaining tissue homeostasis and represents a normal function to eliminate excess or dysfunctional cells. Accumulated evidence suggests that, in healthy women, endometrial cells expelled during menstruation do not survive in ectopic locations because of programmed cell death, while decreased apoptosis may lead to the ectopic survival and implantation of these cells, resulting in the development of endometriosis. Both the inability of endometrial cells to transmit a 'death' signal and the ability of endometrial cells to avoid cell death have been associated with increased expression of anti-apoptotic factors and decreased expression of pre-apoptotic factors. This paper is a review of the recent literature focused on the differential expression of apoptosis-associated molecules in the normal endometria of women without endometriosis, and in the eutopic and ectopic endometria of women with endometriosis. The role of apoptosis in the pathogenesis of endometriosis and the basic and clinical research on the current medical treatment for endometriosis from the view of apoptosis will be discussed.

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Condition tags

endometriosis

MeSH descriptors

Apoptosis Apoptosis Apoptosis Drug Resistance Endometriosis Endometriosis Endometrium Aromatase Inhibitors Aromatase Inhibitors Danazol Danazol Drug Resistance Endometriosis Endometriosis Endometrium Endometrium Estrogen Antagonists Estrogen Antagonists Female Gonadotropin-Releasing Hormone

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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 (100)

Cited by (36)

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