Angiogenesis lymphangiogenesis and neurogenesis in endometriosis

Alison J. Hey‐Cunningham, Alison J Hey-Cunningham, Kathleen M Peters, Hector Barrera-Villa Zevallos, Marina Berbic, Robert Markham, Ian S Fraser
Frontiers in bioscience (Elite edition) · 2013 · vol. E5(3) , pp. 1033–1056 · doi:10.2741/e682 · PMID:23747918 · W2319444795
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review examines the interconnected roles of angiogenesis, lymphangiogenesis, and neurogenesis in the eutopic endometrium and ectopic lesions of endometriosis, which are crucial for disease establishment and symptom generation.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 · read from full text ⓘ

This paper is a review that examines how angiogenesis, lymphangiogenesis, and neurogenesis contribute to endometriosis by supporting ectopic establishment and generating endometriosis-associated symptoms. It synthesizes evidence for these processes as they occur in both eutopic endometrium and ectopic endometriotic lesions, highlighting that their regulation is interconnected and complex. The paper discusses endometriosis pathogenesis in the context of menstrual endometrium reaching the peritoneum, while also noting accumulating evidence that endometriosis has genetic influences and involves cross talk between endometrium and endometriotic lesions. This paper is centrally about endometriosis — it specifically reviews angiogenesis, lymphangiogenesis, and neurogenesis in endometriosis.

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Abstract

Endometriosis is a common, benign gynecological disease affecting 10 - 15% of reproductively aged women. It is characterized by the presence of endometrial-like tissue at sites outside the uterus. The most widely accepted theory of endometriosis pathogenesis proposes that shed menstrual endometrium can reach the peritoneum, implant and grow as endometriotic lesions. Angiogenesis, lymphangiogenesis and neurogenesis are implicated in successful ectopic establishment and the generation of endometriosis-associated symptoms. This review considers these processes as they occur in the eutopic endometrium and ectopic endometriotic lesions of women with endometriosis. Their regulation is inter-connected and complex. Dysregulation in endometriosis occurs on a background of accumulating evidence that endometriosis is an endometrial disease with underlying genetic influences and cross talk with endometriotic lesions. Understanding the roles of angiogenesis, lymphangiogenesis and neurogenesis in endometriosis pathophysiology is essential for the development of novel therapeutic approaches.
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Abstract

Endometriosis is a common, benign gynecological disease affecting 10 – 15% of reproductively aged women. It is characterized by the presence of endometrial-like tissue at sites outside the uterus. The most widely accepted theory of endometriosis pathogenesis proposes that shed menstrual endometrium can reach the peritoneum, implant and grow as endometriotic lesions. Angiogenesis, lymphangiogenesis and neurogenesis are implicated in successful ectopic establishment and the generation of endometriosis-associated symptoms. This review considers these processes as they occur in the eutopic endometrium and ectopic endometriotic lesions of women with endometriosis. Their regulation is interconnected and complex. Dysregulation in endometriosis occurs on a background of accumulating evidence that endometriosis is an endometrial disease with underlying genetic influences and cross talk with endometriotic lesions. Understanding the roles of angiogenesis, lymphangiogenesis and neurogenesis in endometriosis pathophysiology is essential for the development of novel therapeutic approaches.

Keywords

- Angiogenesis - Lymphangiogenesis - Neurogenesis - Endometriosis - Pathogenesis - Endometrium - Endometriotic lesion - Review

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Lymphangiogenesis Neovascularization, Pathologic Neurogenesis Endometriosis Female Humans

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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Cited by (50)

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