Pathological functions of hypoxia in endometriosis

Kuei-Yang Hsiao, Shih-Chieh Lin, Meng-Hsing Wu, Shaw-Jenq Tsai
Frontiers in bioscience (Elite edition) · 2015 · vol. 7(2) , pp. 352–366 · doi:10.2741/e736 · PMID:25553382 · W2317119877
article OA: bronze CC0 ⤵ 32 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Hypoxia induces gene expression regulating the implantation, survival, and maintenance of ectopic endometriotic lesions, contributing to disease pathogenesis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

This review discusses how hypoxia contributes to endometriosis pathogenesis, framing it alongside previously established roles of aberrant estrogen signaling and cyclooxygenase-2-derived prostaglandin E2. It synthesizes evidence that hypoxia can induce expression of downstream genes that regulate implantation, survival, and maintenance of ectopic endometriotic lesions, highlighting pathways involving HIF-1α, leptin, and angiogenesis. The paper’s major limitation is that it is a narrative review summarizing existing studies rather than presenting new experimental results. This paper is centrally about endometriosis — it focuses on pathological functions of hypoxia and related gene regulation in endometriotic lesion establishment and persistence.

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Abstract

Endometriosis is one of the most common gynecological diseases that significantly reduce the life quality of affected women. Research results from the past decade clearly demonstrated that aberrant production of estrogen and cyclooxygenase-2-derived prostaglandin E2 play indispensable roles in the pathogenesis of this disease. However, the etiology of endometriosis remains obscure. Recent evidence reveals a new facet of endometriotic pathogenesis by showing that hypoxia induces the expression of many important downstream genes to regulate the implantation, survival, and maintenance of ectopic endometriotic lesions. These new findings shed lights on future investigations of delineating the etiology of endometriosis and designing new therapeutic strategy for endometriosis.
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Abstract

Endometriosis is one of the most common gynecological diseases that significantly reduce the life quality of affected women. Research results from the past decade clearly demonstrated that aberrant production of estrogen and cyclooxygenase-2-derived prostaglandin E2 play indispensable roles in the pathogenesis of this disease. However, the etiology of endometriosis remains obscure. Recent evidence reveals a new facet of endometriotic pathogenesis by showing that hypoxia induces the expression of many important downstream genes to regulate the implantation, survival, and maintenance of ectopic endometriotic lesions. These new findings shed lights on future investigations of delineating the etiology of endometriosis and designing new therapeutic strategy for endometriosis.

Keywords

- HIF-1α - Endometriosis - Prostaglandin - Cyclooxygenase - Leptin - Angiogenesis - Review

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Hypoxia Cyclooxygenase 2 Cyclooxygenase 2 Endometriosis Endometriosis Estrogens Estrogens Female Humans Hypoxia Hypoxia Leptin Leptin Neovascularization, Pathologic Prostaglandins Prostaglandins

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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.

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