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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1575.)
© 2008 American Heart Association, Inc.

Editorials

VEGF-B Taken to Our Hearts

Specific Effect of VEGF-B in Myocardial Ischemia

Lena Claesson-Welsh

From the Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Sweden.

Correspondence to Lena Claesson-Welsh, Uppsala University, Department of Genetics and Pathology, Rudbeck Laboratory, Dag Hammarskjöldsv. 20, 751 85 Uppsala, Sweden. E-mail Lena.Welsh@genpat.uu.se

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

Vascular endothelial growth factor-B (VEGF-B, see Olofsson et al¹) is one of 5 mammalian VEGF family members, the others being VEGF-A, VEGF-C, VEGF-D, and placental growth factor (PlGF). VEGF-B binds to 1 of the VEGF receptor tyrosine kinases, namely VEGF receptor-1 (VEGFR1, Flt1), but not to VEGFR2 and VEGFR3. In addition, VEGF-A and placental growth factor (PlGF) bind to VEGFR1 with high affinity.² The biology of most of the VEGF family of ligands and receptors has to a considerable extent been sorted out, greatly aided by in vivo analyses of transgenic mice. The remaining enigma has been the role of VEGF-B. In the current issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Li and coworkers show that VEGF-B is uniquely required for myocardial angiogenesis.³ These elegant data make it highly interesting to use VEGF-B therapeutically for treatment of ischemic heart disease.

See accompanying article on page 1614

Analysis of transgenic mouse models has shown that the VEGF family of ligands and receptors in many cases have a critical role in de novo formation of the vasculature. Thus, loss of only 1 allele of vegfa leads to embryonic lethality and arrest in vascular development. Gene inactivation of vegfr2 phenocopies the effects of vegfa, indicating that VEGF-A/VEGFR2 are main regulators of endothelial cell development. Modulation of VEGF-A/VEGFR2 expression during development and disease and the recent successful introduction of inhibitors of VEGF-A/VEGFR2 function in treatment of excessive angiogenesis in cancer and retinopathy,^4–6 have reinforced the notion that this ligand/receptor complex is . . . [Full Text of this Article]

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Arterioscler Thromb Vasc Biol 2008 28: 1614-1620. [Abstract] [Full Text] [PDF]