The genetics and biochemistry of endometriosis

Richard O Burney
Current opinion in obstetrics & gynecology · 2013 · vol. 25(4) , pp. 280–286 · doi:10.1097/gco.0b013e3283630d56 · PMID:23759832 · W2045530523
review OA: closed CC0 ⤵ 30 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review synthesizes recent findings on the genetic and biochemical basis of endometriosis, highlighting inflammation, progesterone resistance, and neuroangiogenesis as key pathophysiological themes.

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Abstract

PURPOSE OF REVIEW: Endometriosis is a common gynecologic disorder characterized by the displacement of endometrial tissue to ectopic locations. Although predisposition to endometriosis is likely multifactorial, a genetic component is evident. The biochemistry of the disorder is an area of active investigation with translational potential. This review synopsizes recent developments regarding the molecular underpinnings of endometriosis. RECENT FINDINGS: Significant advancements in understanding the molecular hallmarks of endometriosis have occurred in recent years. Inflammation, attenuated progesterone action, and neuroangiogenesis constitute emerging themes in the pathophysiology of endometriosis. SUMMARY: Delineation of the biochemical processes involved in endometriosis has important implications for clinical care. The discovery of a sufficiently sensitive and specific biomarker for the nonsurgical detection of endometriosis promises earlier diagnosis and prevention of deleterious sequelae. Understanding the inflammatory cause, attenuated progesterone action at the level of the endometrium, and neuronal sensitization of endometriotic lesions has facilitated development of novel therapeutic approaches for associated pain and infertility.

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Condition tags

endometriosisinfertility

MeSH descriptors

Endometriosis Endometriosis Endometrium Apoptosis Biomarkers Biomarkers Endometriosis Endometrium Female Gene Expression Regulation Humans Infertility, Female Infertility, Female Infertility, Female Inflammation Inflammation Progesterone Progesterone Risk

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 (77)

Cited by (30)

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License: CC0 · commercial use OK