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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:879.)
© 2005 American Heart Association, Inc.

Editorials

Soluble Levels of Receptor for Advanced Glycation Endproducts (sRAGE) and Coronary Artery Disease

The Next C-Reactive Protein?

Barry I. Hudson; Evis Harja; Bernhard Moser; Ann Marie Schmidt

From the Division of Surgical Science, Department of Surgery, College of Physicians & Surgeons, Columbia University, New York.

Correspondence to Ann Marie Schmidt, MD, Division of Surgical Science, Department of Surgery, Columbia University, 630 West 168th Street, P&S 17-501, New York, NY 10032. E-mail ams11@columbia.edu

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

	Introduction

 
The Receptor for advanced glycation endproducts (RAGE) is a multi-ligand member of the immunoglobulin superfamily of cell surface molecules.¹ Although first described as a receptor for AGEs, the products of nonenzymatic glycation and oxidation of proteins/lipids, later studies indicated that RAGE was also a signal transduction receptor for proinflammatory S100/calgranulins and amphoterin (or high mobility group box 1 [HMGB1]) and amyloid-ß–peptide and ß-sheet fibrils.^2–4 Additionally, RAGE is a counter-receptor for Mac-1.⁵ These ligands may be generated and accumulate in diverse settings, such as diabetes, renal failure, neurodegeneration, autoimmunity/inflammatory milieux, and aging. RAGE ligands may synergize in tissues primed by genetic and/or environmental triggers to amplify perturbation. For example, in the case of Mac-1, it was demonstrated that in the presence of S100, the RAGE–Mac-1 interaction was augmented.⁵ Thus, RAGE ligands may be pieces of a scaffold that, together, magnify inflammatory mechanisms in the tissues. If left unchecked, RAGE-mediated sustained inflammation, coupled with failure of regenerative mechanisms, may lead to irreversible tissue injury.¹

See page 1032

	Ligand–RAGE Axis: Breaking the Cycle

 
These concepts have been tested in rodent models of exaggerated neointimal expansion, the hallmark of atherosclerosis and restenosis, triggered by chronic hyperglycemia or acute physical stress. In apolipoprotein E–null mice rendered diabetic with streptozotocin, blockade of RAGE was accomplished using a soluble form of the receptor, soluble (s) RAGE, generated and purified from a baculovirus expression system as a decoy for the families of RAGE ligands. Administration of sRAGE to diabetic apolipoprotein E–null mice suppressed early acceleration of atherosclerosis as well as prevented progression of . . . [Full Text of this Article]

Related Article:

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Arterioscler Thromb Vasc Biol 2005 25: 1032-1037. [Abstract] [Full Text] [PDF]

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