Abstract
Angiogenesis, the generation of new blood vessels, is a ubiquitous process which is tightly regulated in normal physiological situations. The cellular and molecular mechanisms controlling the initiation and termination of the angiogenic process are only partially known (Folkman and Klagsbrun, 1987; Folkman and Shing, 1992; Maragoudakis, 1994; Ferrara, 1996; Montesano et al. , 1996; Pepper et al., 1996). The pathophysiology of many diseases involves uncontrolled growth of new blood vessels, prompting the search for therapeutically effective inhibitors of angiogenesis (Maragoudakis, Sarmonika, and Panoutsacopoulou, 1988; Folkman and Ingber, 1992; Fotsis et al., 1993; D’Amato et al., 1994; O’Reilly et al., 1994; Polverini, 1994; Chen et al., 1995; Gradishar, 1997; O’Reilly et al., 1997). Conversely, in other clinical settings, promotion of neovascularization is desirable, e.g, after myocardial infarction and/or in peripheral blood vessel occlusion, thus calling for appropriate stimulators of “therapeutic” angiogenesis (Höckel et al., 1993; Isner et al., 1995).
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Lelkes, P.I., Hahn, K.A., Karmiol, S., Schmidt, D.H. (1998). Hypoxia/Reoxygenation Enhances Tube Formation of Cultured Human Microvascular Endothelial Cells: the Role of Reactive Oxygen Species. In: Maragoudakis, M.E. (eds) Angiogenesis. NATO ASI Series, vol 298. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9185-3_31
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