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(Circulation Research. 2003;93:87.)
© 2003 American Heart Association, Inc.

Editorials

All in the Family

VEGF-B Joins the Ranks of Proangiogenic Cytokines

Young-sup Yoon, Douglas W. Losordo

From Cardiovascular Research, St Elizabeth’s Medical Center, Boston, Mass.

Correspondence to Douglas W. Losordo, Cardiovascular Research, St Elizabeth’s Medical Center, 736 Cambridge St, Boston, MA 02135. E-mail douglas.losordo@tufts.edu

Key Words: vascular endothelial growth factor-B • vascular endothelial growth factor receptor-1 • VEGFR-1 • angiogenesis • Akt

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

I schemic disease is the leading cause of morbidity and mortality in the United States, accounting for almost 50% of overall mortality,¹ and endothelial dysfunction is a key pathophysiological process that underlies both myocardial and peripheral ischemia. The prevalence of peripheral arterial disease is 12% in the United States, where 150 000 patients undergo lower-limb amputations every year.^2–4 The overall prognosis after amputation is guarded at best, given a perioperative mortality rate of 5% to 20% and 2-year follow-up mortality rate of 40%.³ For those patients who have advanced ischemic cardiac or peripheral vascular diseases and are not suitable for currently available treatment options, such as endovascular intervention or surgical reconstruction, biological revascularization has emerged as a new therapeutic option.⁵

Vasculogenesis and angiogenesis are the mechanisms responsible for the development of the new blood vessels (neovascularization). Angiogenesis refers to the formation of capillaries from preexisting vessels in the embryo and adult organism, whereas vasculogenesis is the development of new blood vessels via differentiation of endothelial progenitor cells or angioblasts in situ.^6,7 Vascular endothelial growth factor (VEGF) family members and their receptors are major mediators of the regulatory machinery that governs these processes both during development and in pathological conditions.⁸ VEGF (or VEGF-A, VEGF-1), a primary regulator of angiogenesis and vasculogenesis,⁹ is a hypoxia-inducible endothelial cell (EC) mitogen,¹⁰ which stimulates EC migration and vessel permeability and promotes EC proliferation and survival of newly formed vessels.¹¹ The family of VEGF-related molecules has recently grown and currently consists of five members: VEGF-A, VEGF-B, . . . [Full Text of this Article]

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				F. Zhang, Z. Tang, X. Hou, J. Lennartsson, Y. Li, A. W. Koch, P. Scotney, C. Lee, P. Arjunan, L. Dong, et al. VEGF-B is dispensable for blood vessel growth but critical for their survival, and VEGF-B targeting inhibits pathological angiogenesis PNAS, April 14, 2009; 106(15): 6152 - 6157. [Abstract] [Full Text] [PDF]

				W.-P. T Ruifrok, R. A de Boer, A. Iwakura, M. Silver, K. Kusano, R. A Tio, and D. W Losordo Estradiol-induced, endothelial progenitor cell-mediated neovascularization in male mice with hind-limb ischemia Vascular Medicine, February 1, 2009; 14(1): 29 - 36. [Abstract] [PDF]