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Wednesday, 06/18/2014 11:12:52 AM

Wednesday, June 18, 2014 11:12:52 AM

Post# of 30990
Angiogenesis: Potentials for Pharmacologic Intervention in the Treatment of Cancer, Cardiovascular Diseases, and Chronic Inflammation in Pharmacological Reviews, Arjan W. Griffioen1,1 and Grietje Molema2, 1Tumor Angiogenesis Laboratory (A.W.G.), Department of Internal Medicine, University Hospital Maastricht, Maastricht; 2Groningen University Institute for Drug Exploration (G.M.), Department of Pathology and Laboratory Medicine, Tumor Immunology Laboratory, and Department of Pharmacokinetics and Drug Delivery, Groningen, The Netherlands, 2000

Abstract:
"Angiogenesis, or the formation of new blood vessels out of pre-existing capillaries, is a sequence of events that is fundamental to many physiologic and pathologic processes such as cancer, ischemic diseases, and chronic inflammation. With the identification of several proangiogenic molecules such as the vascular endothelial cell growth factor, the fibroblast growth factors (like in FGFs), and the angiopoietins, and the recent description of specific inhibitors of angiogenesis such as platelet factor-4, angiostatin, endostatin, and vasostatin, it is recognized that therapeutic interference with vasculature formation offers a tool for clinical applications in various pathologies. Whereas inhibition of angiogenesis can prevent diseases with excessive vessel growth such as cancer, diabetes retinopathy, and arthritis, stimulation of angiogenesis would be beneficial in the treatment of diseases such as coronary artery disease and critical limb ischemia in diabetes. In this review we highlight the current knowledge on angiogenesis regulation and report on the recent findings in angiogenesis research and clinical studies. We also discuss the potentials, limitations, and challenges within this field of research, in light of the development of new therapeutic strategies for diseases in which angiogenesis plays an important role"

Article at:
http://pharmrev.aspetjournals.org/content/52/2/237.full

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