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Arterioscler Thromb Vasc Biol. 2008 Sep;28(9):1614-20. doi: 10.1161/ATVBAHA.107.158725. Epub 2008 May 29.

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

Author information

1
Vesalius Research Center, VIB, 3000 Leuven, Belgium.

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.

PMID:
18511699
PMCID:
PMC2753879
DOI:
10.1161/ATVBAHA.107.158725
[Indexed for MEDLINE]
Free PMC Article

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