Mechanistic and therapeutic implications of angiogenesis in endometriosis

Taylor, Robert N; Yu, Jie; Torres, Paulo B; Schickedanz, Aimee C; Park, John K; Mueller, Michael D; Sidell, Neil (2009). Mechanistic and therapeutic implications of angiogenesis in endometriosis. Reproductive sciences, 16(2), pp. 140-6. Thousand Oaks, Calif.: Sage 10.1177/1933719108324893

Full text not available from this repository.

Like tumor metastases, endometriotic implants require neovascularization to proliferate and invade into ectopic sites within the host. Endometrial tissue, with its robust stem cell populations and remarkable regenerative capabilities, is a rich source of proangiogenic factors. Among the most potent and extensively studied of these proteins, vascular endothelial growth factor has emerged as a critical vasculogenic regulator in endometriosis. Accordingly, angiogenesis of the nascent endometriotic lesion has become an attractive target for novel medical therapeutics and strategies to inhibit vascular endothelial growth factor action. Vascular endothelial growth factor gene regulation in endometrial and endometriosis cells by nuclear receptors, other transcription factors, and also by infiltrating immune cells is emphasized. New data showing that oxidative and endoplasmic reticulum stress increase vascular endothelial growth factor expression are provided. Finally, we review the clinical implications of angiogenesis in this condition and propose potential antiangiogenic therapies that may become useful in the control or eradication of endometriotic lesions.

Item Type:

Journal Article (Further Contribution)

Division/Institute:

04 Faculty of Medicine > Department of Gynaecology, Paediatrics and Endocrinology (DFKE) > Clinic of Gynaecology

UniBE Contributor:

Mueller, Michael

ISSN:

1933-7191

Publisher:

Sage

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 15:12

Last Modified:

05 Dec 2022 14:22

Publisher DOI:

10.1177/1933719108324893

PubMed ID:

19001553

Web of Science ID:

000263386400003

URI:

https://boris.unibe.ch/id/eprint/31593 (FactScience: 196212)

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