Hypoxia: The force of endometriosis

Meng‐Hsing Wu, Meng-Hsing Wu, Wu MH, Kuei-Yang Hsiao, Kuei‐Yang Hsiao, Shaw-Jenq Tsai, Shaw‐Jenq Tsai
Journal of Obstetrics and Gynaecology Research · 2019 · vol. 45(3) , pp. 532–541 · doi:10.1111/jog.13900 · PMID:30618168 · W2909794175
Review OA: closed CC0 ⤵ 62 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

This review summarizes how hypoxia drives ectopic lesion implantation, proliferation, and progression in endometriosis by inducing epigenetic modulation, steroidogenesis, angiogenesis, inflammation, and metabolic changes.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

AIM: Summarize recent findings of how hypoxia regulates numerous important processes to facilitate the implantation, proliferation and progression of ectopic endometriotic lesions. METHODS: Most up-to-date evidences about how hypoxia contributes to the disease pathogenesis of endometriosis and potential therapeutic approaches were collected by conducting a comprehensive search of medical literature electronic databases. Quality of data was analyzed by experienced experts including gynecologist and basic scientists. RESULTS: Uterus is a highly vascularized organ, which makes endometrial cells constantly expose to high concentration of oxygen. When endometrial tissues shed off from the eutopic uterus and retrograde to the peritoneal cavity, they face severe hypoxic stress. Even with successful implantation to ovaries or peritoneum, the hypoxic stress remains as a critical issue because endometrial cells are used to live in the well-oxygenated environment. Under the hypoxia condition, cells undergo epigenetic modulation and evolve several survival processes including steroidogenesis, angiogenesis, inflammation and metabolic switch. The complex gene regulatory network driven by hypoxia ensures endometriotic cells can survive under the hostile peritoneal microenvironment. CONCLUSION: Hypoxia plays critical roles in promoting pathological processes to facilitate the development of endometriosis. Targeting hypoxia-mediated gene network represents an alternative approach for the treatment of endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Endometriosis Hypoxia Neovascularization, Pathologic Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Female Humans Humans Hypoxia Hypoxia Hypoxia Neovascularization, Pathologic Neovascularization, Pathologic Neovascularization, Pathologic

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (100)

Cited by (50)

Source provenance

europepmc
last seen: 2026-10-14T06:08:39.101224+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-10-08T21:23:40.374240+00:00
unpaywall
last seen: 2026-10-14T06:23:58.021457+00:00
License: CC0 · commercial use OK