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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:993.)
© 2007 American Heart Association, Inc.

Editorials

Choking off Plaque Neovascularity

A Promising Atheroprotective Strategy or A Double-Edged Sword?

Kuang-Yuh Chyu; Prediman K. Shah

From the Division of Cardiology and Atherosclerosis Research Center, Department of Medicine and the Burns and Allen Research Institute, Cedars-Sinai Medical Center and the David Geffen School of Medicine at UCLA, Los Angeles, Calif.

Correspondence to Prediman K. Shah, MD, Division of Cardiology, Cedars Sinai Medical Center, Suite 5531, 8700 Beverly Blvd., Los Angeles, CA 90048. E-mail Shahp@cshs.org

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

"For every complex problem there is a simple solution—and it’s wrong."

— H.L. Mencken

Atherosclerosis is a highly prevalent disease that results from a complex interplay between lipids, endothelial cells, immunoinflammatory cells, cytokines, extracellular matrix, and neovascularization.¹ Several lines of evidence suggest that increased adventitial and plaque neovascularity, commonly observed in murine and human atherosclerosis, plays an important role in progression and, possibly, destabilization of atherosclerosis.^1–9 Increased plaque neovascularity may contribute to plaque progression by its link to inflammation, as a source of intraplaque hemorrhage and plaque lipid (Figure).^1,5,7–9

View larger version (21K):   Schematic illustrates the potential mechanisms of plaque neoangiogenesis and its potential role in atherosclerotic plaque progression. The putative mechanism by which oral DNA Vaccine against Flk-1 (fetal liver kinase or VEGFR2)-expressing cells may inhibits angiogenesis and plaque progression is also shown. The red arrows indicate the potential adverse aspects of such a therapeutic strategy. VEGF indicates vascular endothelial growth factor; VEGFR2, vascular endothelial growth factor receptor 2; IL-8, interleukin-8.

See page 1095

The precise mechanisms contributing to increased plaque neovascularity remain to be defined; however, inflammation and one or more angiogenic growth factors have been implicated. One of the pathways for angiogenesis leading to neovascularization involves the family of vascular endothelial growth factor(s) (VEGF) and their receptors (VEGFR). Therefore, VEGF and VEGFR mediated angiogenesis has emerged as a potential target for modulation of atherosclerosis.^3,6 In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Petrovan et al report on a novel approach to inhibiting plaque angiogenesis in hypercholesterolemic mice. . . . [Full Text of this Article]

Related Article:

DNA Vaccination Against VEGF Receptor 2 Reduces Atherosclerosis in LDL Receptor–Deficient Mice

Ramona J. Petrovan, Charles D. Kaplan, Ralph A. Reisfeld, and Linda K. Curtiss
Arterioscler Thromb Vasc Biol 2007 27: 1095-1100. [Abstract] [Full Text] [PDF]

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