Angiogenesis and Endometriosis

Ana Luiza L Rocha,Fernando M Reis,Robert N Taylor

doi:10.1155/2013/859619

Abstract

A comprehensive review was performed to survey the role of angiogenesis in the pathogenesis of endometriosis. This is a multifactorial disease in which the development and maintenance of endometriotic implants depend on their invasive capacity and angiogenic potential. The peritoneal fluid of patients with endometriosis is a complex suspension carrying inflammatory cytokines, growth factors, steroid hormones, proangiogenic factors, macrophages, and endometrial and red blood cells. These cells and their signaling products concur to promote the spreading of new blood vessels at the endometriotic lesions and surroundings, which contributes to the endometriotic implant survival. Experimental studies of several antiangiogenic agents demonstrated the regression of endometriotic lesions by reducing their blood supply. Further studies are necessary before these novel agents can be introduced into clinical practice, in particular the establishment of the safety of anti-angiogenic medications in women who are seeking to become pregnant.

Highlights

Endometriosis is a benign sex hormone-dependent gynecological disease, characterized by the presence and growth of endometrial tissue outside the uterus; it affects 10% of women of reproductive age and is associated with infertility and pain [1, 2]
The aim of this paper is to review the literature evidence of the important role of angiogenesis in the pathogenesis of endometriosis and to establish the rationale for antiangiogenic agents as a new therapeutic option in the treatment of endometriosis patients
Endometriotic lesions are typically characterized by a dense vascularization that occurs through angiogenesis process [1, 9, 14]

Summary

Introduction

Endometriosis is a benign sex hormone-dependent gynecological disease, characterized by the presence and growth of endometrial tissue outside the uterus; it affects 10% of women of reproductive age and is associated with infertility and pain [1, 2]. The disease derives from retrograde menstruation of endometrial cells which implant on peritoneal surfaces and induce an inflammatory response. The success of the ectopic implants depends on other pathological processes such as neoangiogenesis, fibrosis, adhesion formation, avoidance of apoptosis, immune dysfunction, and neuronal infiltration [1, 2, 4,5,6,7]. Cyclic angiogenesis is orchestrated by the endocrine system, providing physiological signals for follicular maturation, corpus luteum function, endometrial growth, and remodeling [8]. Endometriotic lesions require an adequate blood supply to survive in their ectopic sites

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