ANGIOGENESIS OF THE ENDOMETRIUM

Ovadia Abulafia, David M. Sherer
In: Obstetrics & Gynecology · 1999 · vol. 94(1) , pp. 148–153 · doi:10.1097/00006250-199907000-00031 · W4239238531
article OA: closed CC0 ⤵ 6 in-corpus citations
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-07-14 ⓘ

This review examines current data on endometrial angiogenesis during the normal menstrual cycle and in benign and neoplastic endometrial diseases, concluding it actively participates in both normal regeneration and pathological conditions.

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This review synthesizes data from human and animal studies regarding endometrial angiogenesis during the normal menstrual cycle and in various pathological states. The authors identify that angiogenic processes are critical for cyclic regeneration as well as for conditions such as dysfunctional uterine bleeding, leiomyomata, hyperplasia, and carcinoma. They note that understanding these specific patterns could eventually enhance the use of antiangiogenic therapies for both benign and neoplastic endometrial diseases. Relevance to endometriosis: listed among other conditions influenced by endometrial angiogenesis, though the paper's main focus is a broad overview of endometrial vascular changes rather than deep dive into endometriosis pathophysiology.

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Abstract

In Brief Objective To present current data pertaining to angiogenesis of the endometrium throughout the normal menstrual cycle and in benign and neoplastic diseases of the endometrium. Sources We conducted a computerized search of MEDLINE, Current Contents, and Index Medicus for relevant studies in the English literature published between January 1966 and October 1998. Study selection We reviewed all studies that included human and animal models of angiogenesis of normal cyclic endometrium and benign and neoplastic endometrial diseases. Tabulation, Integration, and Results Angiogenesis is important to cyclic, regenerating endometria and disease processes including dysfunctional uterine bleeding, response to exogenous hormonal treatment, bleeding associated with intrauterine contraceptive devices, uterine leiomyomata, endometriosis, complex endometrial hyperplasia, and endometrial carcinoma. Conclusion In the future, knowledge of specific angiogenic patterns of various disease processes might improve application of antiangiogenic medications in therapies for benign and neoplastic diseases of the endometrium. Angiogenesis actively participates in the development of normal cyclic regenerating endometrium and in a wide spectrum of benign and malignant pathologic conditions of the endometrium.
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Objective

To present current data pertaining to angiogenesis of the endometrium throughout the normal menstrual cycle and in benign and neoplastic diseases of the endometrium. Sources We conducted a computerized search of MEDLINE, Current Contents, and Index Medicus for relevant studies in the English literature published between January 1966 and October 1998. Study selection We reviewed all studies that included human and animal models of angiogenesis of normal cyclic endometrium and benign and neoplastic endometrial diseases. Tabulation, Integration, and Results Angiogenesis is important to cyclic, regenerating endometria and disease processes including dysfunctional uterine bleeding, response to exogenous hormonal treatment, bleeding associated with intrauterine contraceptive devices, uterine leiomyomata, endometriosis, complex endometrial hyperplasia, and endometrial carcinoma.

Conclusion

In the future, knowledge of specific angiogenic patterns of various disease processes might improve application of antiangiogenic medications in therapies for benign and neoplastic diseases of the endometrium.

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Condition tags

endometriosis

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 (44)

Cited by (6)

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