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(Circulation Research. 2008;103:903.)
© 2008 American Heart Association, Inc.

Editorials

The Renaissance of Vascular Endothelial Growth Factor, Part B

Wolfgang Schaper

From the Max-Planck-Institute for Heart and Lung Research, Experimental Cardiology, Arteriogenesis Research Group, Bad Nauheim, Germany.

Correspondence to Prof Wolfgang Schaper, Max-Planck-Institute for Heart and Lung Research, Experimental Cardiology, Arteriogenesis Research Group, Sprudelhof 11, Bad Nauheim, He D-61231, Germany. E-mail w.schaper@kerckhoff.mpg.de

Key Words: lipid metabolites • blood flow • cardiomyopathy • cardiac hypertrophy

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Almost 20 years ago, in 1989, 2 independent research groups reported their discoveries of a new peptide that increased vascular permeability and stimulated endothelial cells to divide.^1,2 The proposed name of the peptides, vascular permeability factor, was later changed to vascular endothelial growth factor (VEGF). A year later Clauss et al³ showed that VEGF was a chemoattractant for monocytes, a finding that greatly interested me because my colleagues and I had shown, much earlier, that monocytes played an important role in coronary arteriogenesis,^4,5 the process by which ischemic myocardium produced an arterial bypass circulation that circumvents occlusions and salvages ischemic myocardium. VEGF was a significant contributor to the emerging field of angiogenesis that was promoted by the late Judah Folkman⁶ and had been dominated, up to that time, by research on the fibroblast growth factor (FGF) family.⁷ That VEGF was regulated by the oxygen availability of the tissue^8,9 strengthened the belief that ischemia, a consequence of arterial occlusions, was the key factor for all vascular adaptations that tried to improve tissue perfusion. On the other hand, inhibition of VEGF production could in principle starve cancers to death. Thus, VEGF research nourished the hope that the scourge of mankind, atherosclerosis and cancer, could be cured from 1 and the same principle: stimulation or inhibition of VEGF. An enormous wave of research began, especially when the groups of Carmeliet and Risau¹⁰ and Ferrara¹¹ showed that even heterozygote knockouts were not viable, underscoring the central role that VEGF played in the development of . . . [Full Text of this Article]