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Reproductive Sciences
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*Endometriosis
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Mechanistic and Therapeutic Implications of Angiogenesis in Endometriosis

Robert N. Taylor, MD, PhD

Department of Gynecology and Obstetrics, Human Uterine Biology Program, Emory University School of Medicine, Atlanta, Georgia, robert.n.taylor{at}emory.edu

Jie Yu, MD, MSc

Department of Gynecology and Obstetrics, Human Uterine Biology Program, Emory University School of Medicine, Atlanta, Georgia

Paulo B. Torres, MD

Department of Gynecology and Obstetrics, Human Uterine Biology Program, Emory University School of Medicine, Atlanta, Georgia

Aimee C. Schickedanz, MD

Department of Gynecology and Obstetrics, Human Uterine Biology Program, Emory University School of Medicine, Atlanta, Georgia

John K. Park, MD, MSc

Department of Gynecology and Obstetrics, Human Uterine Biology Program, Emory University School of Medicine, Atlanta, Georgia

Michael D. Mueller, MD

Department of Gynecology and Obstetrics, Human Uterine Biology Program, Emory University School of Medicine, Atlanta, Georgia

Neil Sidell, PhD

Department of Gynecology and Obstetrics, Human Uterine Biology Program, Emory University School of Medicine, Atlanta, Georgia

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.

Key Words: VEGF • uterus • endothelial.

This version was published on February 1, 2009

Reproductive Sciences, Vol. 16, No. 2, 140-146 (2009)
DOI: 10.1177/1933719108324893


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