(Circulation. 1996;94:1496-1498.)
© 1996 American Heart Association, Inc.
Articles |
Use of Vascular Endothelial Growth Factor for Therapeutic Angiogenesis
the Vascular Cell Biology Laboratory, Texas Heart Institute, Houston, and the Department of Internal Medicine, Division of Cardiology, University of Texas Medical School, Houston.
Correspondence to David Engler, PhD, Texas Heart Institute, Vascular Cell Biology, PO Box 20345 MC 2-255, Houston, TX 77225-0345. E-mail dengler@biost1.thi.tmc.edu.
Key Words: Editorials • growth substances • receptors • revascularization
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Introduction |
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The term "therapeutic angiogenesis" was coined to describe intervention used to treat or prevent pathological clinical situations characterized by local hypovascularity by stimulating or inducing neovascularization.1 Angiogenesis is defined as the formation of new blood vessels from preexisting vessels by the process of cellular outgrowth. Angiogenesis differs from vasculogenesis, which is an embryonic phenomenon in which new blood vessels are formed de novo from blood islands composed of committed stem cells. Therefore, angiogenesis accounts for all new vessel growth after embryonic life and is a normal function of such processes as injury repair and the female reproductive cycle. The angiogenic process requires a concerted series of events. These include the migration and proliferation of endothelial cells in and away from the original microvasculature, the breakdown of basement membranes and the controlled expression of proteolytic enzymes that can degrade extracellular matrices, the reassembly of new extracellular matrix, and endothelial tube formation. Under certain circumstances, insufficient angiogenesis can lead to such problems as ulcers that do not heal and myocardial infarction. Conversely, many pathologies are complicated by unregulated angiogenesis and are typified by cancer, diabetic retinopathy, and atherosclerosis itself (see below).
The normal process of angiogenesis is controlled by the balance of proangiogenic and antiangiogenic molecules that are spatially and temporally regulated in vivo (reviewed in Reference 2 and references cited there). In addition to VEGF, proangiogenic molecules include members of the FGF family, transforming growth factor-ß, tumor necrosis factor-
, platelet-derived growth factor-BB, and others. These soluble molecules exert their angiogenic
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