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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:965.)
© 2006 American Heart Association, Inc.

Editorials

A New Dimension in the Vasculoprotective Function of HDL

Progenitor-Mediated Endothelium Repair

Philippe Lesnik; M. John Chapman

From the Dyslipidemia and Atherosclerosis Research Unit, National Institute for Health and Medical Research (INSERM), University Pierre et Marie Curie, Hôpital de la Pitié, Paris, France.

Correspondence to M. John Chapman, PhD, DSc, Dyslipidemia and Atherosclerosis Research Unit, INSERM U551, Hôpital de la Pitié, 83, Blvd de l’hôpital, 75651 Paris cedex 13, France. E-mail Chapman@chups.jussieu.fr

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

	Introduction

 
Although the vascular endothelium is a potent antithrombotic, antioxidant, and antiinflammatory barrier, prolonged and repeated exposure to the oxidative stress and chronic inflammation which are intimately associated with cardiovascular risk factors such as hypercholesterolemia, hyperglycemia, hypertension, low shear stress, and smoking ultimately blunts these protective mechanisms. Under these conditions, the endothelium not only becomes dysfunctional, but equally may undergo apoptosis resulting in cellular detachment from the underlying intimal layer. Endothelial dysfunction is a key precocious event in the pathogenesis of atherosclerosis and critically contributes to plaque initiation and progression. Denudation of endothelium is associated with increase in proliferation of vascular smooth muscle cells, enhanced recruitment of monocytes, lipid deposition, and inflammation leading to neointima formation and increased risk of thrombosis. Indeed, thrombi can be formed on denuded endothelial plaque surfaces as well as on apoptotic endothelial cells.¹

See page 1144

Mechanisms implicated in endothelial dysfunction include attenuated nitric oxide generation and bioavailability, oxidative stress, upregulation of adhesion molecule expression, generation of chemokines such as macrophage chemoattractant protein-1, and production of plasminogen activator inhibitor (PAI)-1; all of these factors contribute directly or indirectly to the inflammatory response and equally to the development of a prothrombic state. In addition, numerous studies support the concept that impaired endothelium-dependent vasodilation reflects major alteration in endothelial function. Indeed, endothelium-derived nitric oxide (NO), synthesized by NO synthase (eNOS) from its precursor L-arginine, is a major mediator of endothelium-dependent vasodilation and is critically involved in the regulation of other protective properties of the healthy endothelium.²

	HDL and Vascular Protection

 
Atherosclerosis risk . . . [Full Text of this Article]

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Arterioscler Thromb Vasc Biol 2006 26: 1144-1149. [Abstract] [Full Text] [PDF]

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