How transcription factors regulate apoptosis in endometriosis (Review)

Zhuqing Ouyang, Juexiao Deng, Lanyue Zhang, Fujin Shen
Molecular medicine reports · 2025 · vol. 32(5) , pp. 1–11 · doi:10.3892/mmr.2025.13654 · PMID:40849823 · PMC12382432 · W4413297129
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review summarizes how transcription factors regulate apoptosis in endometriosis pathogenesis, identifying potential therapeutic targets and biomarkers for this disease.

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

This paper is a review examining how transcription factors regulate apoptosis in endometriosis, focusing on transcription factor EB (TFEB), NF-κB, and FOXO1, and also discussing additional regulators and signaling pathways. Across described studies, apoptosis is suppressed in endometriosis lesions—e.g., with increased Bcl-2 and decreased Bax and Fas—such that failure of programmed cell death supports ectopic endometrial survival and lesion development; a key example is TFEB upregulation, which is reported to increase autophagic flux (including LC3 and Beclin1 changes), elevate cell viability, and inhibit caspase-3 cleavage, with effects reduced by the autophagy inhibitor chloroquine. The review notes mechanistic complexity and includes explicit contradictions, such as reports that high mTOR/AKT in endometriosis would prevent autophagy and TFEB activation via classical routes, implying additional non-mTOR pathways like ROS-driven TRPML1/Ca2+-dependent TFEB dephosphorylation. This paper is centrally about endometriosis — it synthesizes evidence linking transcription-factor control of apoptosis and autophagy (notably via TFEB) to the formation and progression of endometriotic lesions.

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Abstract

Endometriosis (EM) is a common chronic gynaecological disease that affects 10% of women of reproductive age globally. EM is defined as the presence of endometrial glands and stroma in extrauterine locations, and it can result in pelvic pain and infertility. Inflammation, oxidative stress and apoptosis dysregulation serve a key role in endometriotic lesions. The pathogenesis of EM remains unclear, posing major clinical challenges in its diagnosis and treatment. Apoptosis contributes to the maintenance of cellular homeostasis during the menstrual cycle by eliminating ageing cells from the functional layer of the uterine endometrium. Inhibition of apoptosis facilitates ectopic endometrial cell invasion, implantation and survival, and it promotes the occurrence and development of EM. Transcription factors are pivotal regulators of cellular processes and serve key roles in regulating apoptosis to promote EM. Therefore, identifying the mechanisms by which transcription factors regulate apoptosis in EM may help identify novel targets for the treatment of this disease. The present review summarizes the regulation of apoptosis by different transcription factors in the pathogenesis of EM, contributing to the development of promising biomarkers and therapeutic strategies.

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Condition tags

endometriosisinfertility

MeSH descriptors

Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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 (100)

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