Anti-angiogenic treatment strategies for the therapy of endometriosis.
BACKGROUND Angiogenesis, i.e. the development of new blood vessels from pre-existing ones, represents an integral part in the pathogenesis of endometriosis. During the last decade, an increasing number of studies have therefore focused on the anti-angiogenic treatment of the disease. The present review provides a systematic overview of these studies and critically discusses the future role of anti-angiogenic therapy in the multimodal management of endometriosis.  METHODS Literature searches were performed in PubMed, MEDLINE and ISI Web of Knowledge for original articles published before the end of March 2012, written in the English language and focusing on anti-angiogenic approaches for the therapy of endometriosis. The searches included both animal and human studies.  RESULTS Numerous compounds of different substance groups have been shown to exert anti-angiogenic effects on endometriotic lesions under experimental in vitro and in vivo conditions. These include growth factor inhibitors, endogenous angiogenesis inhibitors, fumagillin analogues, statins, cyclo-oxygenase-2 inhibitors, phytochemical compounds, immunomodulators, dopamine agonists, peroxisome proliferator-activated receptor agonists, progestins, danazol and gonadotropin-releasing hormone (GnRH) agonists. However, clinical evidence for their efficacy in anti-angiogenic endometriosis therapy is still lacking.  CONCLUSIONS Anti-angiogenic compounds hold great promise for the future treatment of endometriosis because they may inhibit the establishment of new endometriotic lesions in early stages of the disease or after surgical treatment. Further experimental studies, controlled clinical trials in particular, are required now to clarify which compounds fulfil these expectations without inducing severe side effects in patients with endometriosis.
Institute for Clinical & Experimental Surgery, University of Saarland, Homburg/Saar, Germany. matthias.laschke@uks.eu
M W
MW
Laschke
M D
MD
Menger
D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D043165:Angiostatic Proteins / Q000627:therapeutic use; D003510:Cyclohexanes / Q000627:therapeutic use; D052246:Cyclooxygenase 2 Inhibitors / Q000627:therapeutic use; D018491:Dopamine Agonists / Q000627:therapeutic use; D004715:Endometriosis / Q000188:drug therapy* / Q000473:pathology; D005231:Fatty Acids, Unsaturated / Q000627:therapeutic use; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007155:Immunologic Factors / Q000627:therapeutic use; D047492:Peroxisome Proliferator-Activated Receptors / Q000819:agonists; D008517:Phytotherapy; D012717:Sesquiterpenes / Q000627:therapeutic use; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors
D020533:Angiogenesis Inhibitors; D043165:Angiostatic Proteins; D003510:Cyclohexanes; D052246:Cyclooxygenase 2 Inhibitors; D018491:Dopamine Agonists; D005231:Fatty Acids, Unsaturated; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007155:Immunologic Factors; D047492:Peroxisome Proliferator-Activated Receptors; D012717:Sesquiterpenes; D042461:Vascular Endothelial Growth Factor A; C026211:fumagillin