title: Vascular endothelial growth factor and endometriotic angiogenesis.
abstract: Peritoneal endometriosis is a significant debilitating gynaecological problem of widespread prevalence. It is now generally accepted that the pathogenesis of peritoneal endometriosis involves the implantation of exfoliated endometrium. Essential for its survival is the generation and maintenance of an extensive blood supply both within and surrounding the ectopic tissue. The vascular endothelial growth factor (VEGF) family of angiogenic molecules is involved in both physiological angiogenesis, and a number of pathological conditions that are characterized by excessive angiogenesis. Increasing evidence suggests that the VEGF family may also be involved with both the aetiology and maintenance of peritoneal endometriosis. Sources of this factor include the eutopic endometrium, ectopic endometriotic tissue and peritoneal fluid macrophages. Important to its aetiology is the correct peritoneal environment in which the exfoliated endometrium is seeded and implants. Established ectopic tissue is then dependent on the peritoneal environment for its survival, an environment that supports angiogenesis. Our increasing knowledge of the involvement of the VEGF family in endometriotic angiogenesis raises the possibility of novel approaches to its medical management, with particular focus on the anti-angiogenic control of the action of VEGF.
authors.affiliation: Department of Obstetrics and Gynaecology, University of Leicester, Faculty of Medical and Biological Sciences, UK.
authors.forename: J
authors.initials: J
authors.lastname: McLaren
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D001202:Ascitic Fluid / Q000166:cytology; D015815:Cell Adhesion Molecules / Q000378:metabolism; D004715:Endometriosis / Q000209:etiology* / Q000473:pathology; D004717:Endometrium / Q000098:blood supply* / Q000473:pathology; D016228:Endothelial Growth Factors / Q000494:pharmacology / Q000502:physiology*; D005260:Female; D006801:Humans; D008222:Lymphokines / Q000494:pharmacology / Q000502:physiology*; D009389:Neovascularization, Pathologic; D018919:Neovascularization, Physiologic; D020794:Receptor Protein-Tyrosine Kinases / Q000187:drug effects / Q000502:physiology; D017978:Receptors, Growth Factor / Q000187:drug effects / Q000502:physiology; D040262:Receptors, Vascular Endothelial Growth Factor; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
chemical_list: D020533:Angiogenesis Inhibitors; D015815:Cell Adhesion Molecules; D016228:Endothelial Growth Factors; D008222:Lymphokines; D017978:Receptors, Growth Factor; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D020794:Receptor Protein-Tyrosine Kinases; D040262:Receptors, Vascular Endothelial Growth Factor