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Reevaluation of the role of VEGF-B suggests a restricted role in the revascularization of the ischemic myocardium.

by Xuri Li, Marc Tjwa, Inge Van Hove, Berndt Enholm, Elke Neven, Karri Paavonen, Michael Jeltsch, Toni Diez Juan, Richard E Sievers, Emmanuel Chorianopoulos, Hiromichi Wada, Maarten Vanwildemeersch, Agnes Noel, Jean-Michel Foidart, Matthew L Springer, Georges Von Degenfeld, Mieke Dewerchin, Helen M Blau, Kari Alitalo, Ulf Eriksson, Peter Carmeliet, Lieve Moons show all authors
Arteriosclerosis thrombosis and vascular biology (2008)

Abstract

OBJECTIVE: The endogenous role of the VEGF family member vascular endothelial growth factor-B (VEGF-B) in pathological angiogenesis remains unclear. METHODS AND RESULTS: We studied the role of VEGF-B in various models of pathological angiogenesis using mice lacking VEGF-B (VEGF-B(-/-)) or overexpressing VEGF-B(167). After occlusion of the left coronary artery, VEGF-B deficiency impaired vessel growth in the ischemic myocardium whereas, in wild-type mice, VEGF-B(167) overexpression enhanced revascularization of the infarct and ischemic border zone. By contrast, VEGF-B deficiency did not affect vessel growth in the wounded skin, hypoxic lung, ischemic retina, or ischemic limb. Moreover, VEGF-B(167) overexpression failed to enhance vascular growth in the skin or ischemic limb. CONCLUSIONS: VEGF-B appears to have a relatively restricted angiogenic activity in the ischemic heart. These insights might offer novel therapeutic opportunities.

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