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J Am Coll Cardiol, 2007; 49:1015-1026, doi:10.1016/j.jacc.2006.09.053 (Published online 23 February 2007).
© 2007 by the American College of Cardiology Foundation
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STATE-OF-THE-ART PAPER

Vascular Endothelial Growth Factors

Biology and Current Status of Clinical Applications in Cardiovascular Medicine

Seppo Ylä-Herttuala, MD, PhDFESC*,{dagger},§,*, Tuomas T. Rissanen, MD, PhD*, Ismo Vajanto, MD{ddagger} and Juha Hartikainen, MD, PhD{dagger}

* Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute, Kuopio University
{dagger} Department of Medicine
{ddagger} Department of Surgery, Kuopio University and Kuopio University Hospital
§ Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

Manuscript received April 17, 2006; revised manuscript received September 22, 2006, accepted September 27, 2006.

* Address for correspondence: Dr. Seppo Ylä-Herttuala, Professor of Molecular Medicine, Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute, University of Kuopio, P.O. Box 1627, FIN-70211 Kuopio, Finland. (Email: seppo.ylaherttuala{at}uku.fi).

Members of the vascular endothelial growth factor (VEGF) family are among the most powerful modulators of vascular biology. They regulate vasculogenesis, angiogenesis, and vascular maintenance during embryogenesis and in adults. Because of their profound effects on blood vessels, VEGFs have received much attention regarding their potential therapeutic use in cardiovascular medicine, especially for therapeutic vascular growth in myocardial and peripheral ischemia. However, completed randomized controlled VEGF trials have not provided convincing evidence of clinical efficacy. On the other hand, recent preclinical proangiogenic VEGF studies have given insight, and anti-VEGF studies have shown that the disturbance of vascular homeostasis by blocking VEGF-A may lead to endothelial dysfunction and adverse vascular effects. Excess VEGF-A may contribute to neovascularization of atherosclerotic lesions but, currently, there is no evidence that transient overexpression by gene transfer could lead to plaque destabilization. Here, we review the biology and effects of VEGFs as well as the current status of clinical applications and future perspectives of the therapeutic use of VEGFs in cardiovascular medicine.

Abbreviations and Acronyms
  CAD = coronary artery disease
  CCS = Canadian Cardiovascular Society
  CLI = critical limb ischemia
  EC = endothelial cell
  NO = nitric oxide
  PAD = peripheral arterial disease
  PlGF = placental growth factor
  pu = particle units
  SMC = smooth muscle cell
  VEGF = vascular endothelial growth factor
  VEGFR = VEGF receptor




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