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(Circulation Research. 2006;99:787.)
© 2006 American Heart Association, Inc.

Editorials

Plaque Angiogenesis Versus Compensatory Arteriogenesis in Atherosclerosis

Chu-Huang Chen, Jeffrey P. Walterscheid

From the Department of Medicine, Baylor College of Medicine (C.-H.C., J.P.W.), Houston, Tex.

Correspondence to Chu-Huang Chen, Baylor College of Medicine, 6565 Fannin Street, MS A-601, Houston, Texas 77030. E-mail cchen@bcm.tmc.edu

See related article, pages 900–908

Key Words: atherosclerosis • angiogenesis • arteriogenesis • oxidized phospholipids • VEGF • FGF2

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

Many atherosclerotic lesions are vascularized by a network of capillaries that arise from the adventitial vasa vasorum.¹ These capillaries may be important regulators of plaque instability. Reflecting their inflammatory microenvironment, the capillaries are immature endothelial tubes with disorganized branching, fragile and prone to rupture. The accumulation of erythrocytes after intraplaque hemorrhage may promote the transition from lesion stability to instability.²

Research interest in both angiogenesis and arteriogenesis, the maturation or de novo growth of collateral vessels,^3,4 in atherosclerotic disease has intensified in recent years, reflecting the emerging success of antiangiogenesis strategies in cancer therapy. The bench-to-bedside milepost was reached in February 2004, when the US Food and Drug Administration approved bevacizumab (Avastin, Genentech), an anti-vascular endothelial growth factor (VEGF) monoclonal antibody, for the treatment of colorectal cancer.⁵ It is controversial whether angiogenesis-targeted therapy holds similar promise in atherosclerotic disease.³ It must be remembered, however, that it has been 35 years since Folkman published his then-heretical hypothesis that tumor growth depended on angiogenesis,⁶ and 30 years since Brem and Folkman reported the first-known angiogenesis inhibitor.⁷ Many of the complex, multigene events of angiogenesis and arteriogenesis in atherosclerotic disease remain to be elucidated. The challenge is all the more difficult because of the diverse pathophysiological mechanisms of those two major kinds of new vascular growth associated with lesion development, one composed mainly of new capillaries, the other the collateral circulation formed by capillaries, arterioles, and arteries.^2,4

Bochkov and colleagues in the current issue of Circulation Research distinguish new mechanisms of angiogenesis in . . . [Full Text of this Article]

Related Article:

Oxidized Phospholipids Stimulate Angiogenesis Via Autocrine Mechanisms, Implicating a Novel Role for Lipid Oxidation in the Evolution of Atherosclerotic Lesions

Valery N. Bochkov, Maria Philippova, Olga Oskolkova, Alexandra Kadl, Alexander Furnkranz, Erduan Karabeg, Taras Afonyushkin, Florian Gruber, Johannes Breuss, Alexander Minchenko, Diana Mechtcheriakova, Philipp Hohensinner, Kathrin Rychli, Johann Wojta, Therese Resink, Paul Erne, Bernd R. Binder, and Norbert Leitinger
Circ. Res. 2006 99: 900-908. [Abstract] [Full Text] [PDF]

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