Reevaluation of the role of VEGF-B suggests a restricted role in the revascularization of the ischemic myocardium. Li, X., Tjwa, M., Van Hove, I., Enholm, B., Neven, E., Paavonen, K., Jeltsch, M., Juan, T. D., Sievers, R. E, Chorianopoulos, E., Wada, H., Vanwildemeersch, M., Noel, A., Foidart, J., Springer, M. L, von Degenfeld, G., Dewerchin, M., Blau, H. M, Alitalo, K., Eriksson, U., Carmeliet, P., & Moons, L. Arteriosclerosis, Thrombosis, and Vascular Biology, 28(9):1614–1620, September, 2008.
Reevaluation of the role of VEGF-B suggests a restricted role in the revascularization of the ischemic myocardium [link]Paper  doi  abstract   bibtex   
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.
@article{li_reevaluation_2008,
	title = {Reevaluation of the role of {VEGF}-{B} suggests a restricted role in the revascularization of the ischemic myocardium},
	volume = {28},
	issn = {1524-4636},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/18511699},
	doi = {10.1161/ATVBAHA.107.158725},
	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.},
	number = {9},
	urldate = {2012-02-23},
	journal = {Arteriosclerosis, Thrombosis, and Vascular Biology},
	author = {Li, Xuri and Tjwa, Marc and Van Hove, Inge and Enholm, Berndt and Neven, Elke and Paavonen, Karri and Jeltsch, Michael and Juan, Toni Diez and Sievers, Richard E and Chorianopoulos, Emmanuel and Wada, Hiromichi and Vanwildemeersch, Maarten and Noel, Agnes and Foidart, Jean-Michel and Springer, Matthew L and von Degenfeld, Georges and Dewerchin, Mieke and Blau, Helen M and Alitalo, Kari and Eriksson, Ulf and Carmeliet, Peter and Moons, Lieve},
	month = sep,
	year = {2008},
	pmid = {18511699},
	keywords = {Angiogenesis Inducing Agents, Animals, Coronary Vessels, Disease Models, Animal, GENE therapy, Gene Transfer Techniques, Hindlimb, Ischemia, Lung, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Nude, Muscle, Skeletal, Myocardial Ischemia, Myocardium, Neovascularization, Physiologic, Recombinant Proteins, Retinal Vessels, Skin, Up-Regulation, Vascular Endothelial Growth Factor B, Vascular Endothelial Growth Factor Receptor-1},
	pages = {1614--1620},
}

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