Molecular mechanism of autophagy and apoptosis in endometriosis: Current understanding and future research directions

Hiroshi Kobayashi, Shogo Imanaka, Chiharu Yoshimoto, Sho Matsubara, Hiroshi Shigetomi
Reproductive medicine and biology · 2024 · vol. 23(1) , pp. e12577 · doi:10.1002/rmb2.12577 · PMID:38645639 · W4394980772
article OA: gold CC0 ⤵ 18 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review explores how autophagy pathways, influenced by factors like mTOR, hypoxia, and iron, contribute to the survival of endometriotic cells by modulating apoptosis.

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Abstract

Background: Endometriosis is a common gynecological condition, with symptoms including pain and infertility. Regurgitated endometrial cells into the peritoneal cavity encounter hypoxia and nutrient starvation. Endometriotic cells have evolved various adaptive mechanisms to survive in this inevitable condition. These adaptations include escape from apoptosis. Autophagy, a self-degradation system, controls apoptosis during stress conditions. However, to date, the mechanisms regulating the interplay between autophagy and apoptosis are still poorly understood. In this review, we summarize the current understanding of the molecular characteristics of autophagy in endometriosis and discuss future therapeutic challenges. Methods: A search of PubMed and Google Scholar databases were used to identify relevant studies for this narrative literature review. Results: Autophagy may be dynamically regulated through various intrinsic (e.g., PI3K/AKT/mTOR signal transduction network) and extrinsic (e.g., hypoxia and iron-mediated oxidative stress) pathways, contributing to the development and progression of endometriosis. Upregulation of mTOR expression suppresses apoptosis via inhibiting the autophagy pathway, whereas hypoxia or excess iron often inhibits apoptosis via promoting autophagy. Conclusion: Endometriotic cells may have acquired antiapoptotic mechanisms through unique intrinsic and extrinsic autophagy pathways to survive in changing environments.

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Condition tags

endometriosisinfertility

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.

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