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Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:257-266
Published online before print December 1, 2005, doi: 10.1161/01.ATV.0000198239.41189.5d
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:257.)
© 2006 American Heart Association, Inc.


Brief Reviews

Influence of Cardiovascular Risk Factors on Endothelial Progenitor Cells

Limitations for Therapy?

Nikos Werner; Georg Nickenig

From the Medizinischen Klinik und Poliklinik II, Universitätsklinikum Bonn, Germany.

Correspondence to Georg Nickenig, MD, Medizinischen Klinik und Poliklinik II, Universitätsklinikum Bonn, Sigmund-Freud-Straße 25, D-53105 Bonn, Germany. E-mail georg.nickenig{at}ukb.uni-bonn.de

Series Editor: Stephanie Dimmeler
Novel Mediators and Mechanisms in Angiogenesis and Vasculogenesis
ATVB In Focus

Previous Brief Review in this Series:

•Ferguson JE III, Kelley RW, Patterson C. Mechanisms of endothelial differentiation in embryonic vasculogenesis. 2005;25:2246–2254.

The ideal way to prevent and cure atherosclerosis and the subsequent end organ damage is to restore and rejuvenate the dysfunctional vasculature and the damaged organs. Various studies have underlined the important role of bone marrow–derived endothelial progenitor cells (EPCs) in vasculogenesis and angiogenesis of ischemic tissue, but only a few studies have concentrated on the role of EPCs in the prevention and therapy of atherosclerosis. Extended endothelial cell damage by cardiovascular risk factors can result in endothelial cell apoptosis with loss of the integrity of the endothelium. The consequences are an increased vascular permeability of the endothelium followed by facilitated migration of monocytes and vascular smooth muscle cell proliferation, resulting in the premature manifestation of an atherosclerotic lesion. A growing body of evidence suggests that circulating EPCs play an important role in endothelial cell regeneration. Systemic transfusion or intrinsic mobilization of EPCs enhances the restoration of the endothelium after focal endothelial denudation, resulting in a diminished neointima formation. In mice with atherosclerotic lesions, bone-marrow–derived stem cells are able to reduce atherosclerotic plaque size. However, various studies have demonstrated that in humans, cardiovascular risk factors impair number and function of EPCs, potentially restricting the therapeutic potential of progenitor cells. The current review focuses on the role of cardiovascular risk factors on endothelial cell apoptosis and EPCs with its pathophysiological consequences for atherogenesis and a regenerative therapy approach and will highlight the role of EPCs as a marker for cardiovascular mortality and morbidity.

Circulating endothelial progenitor cells play an important role in restoration of the endothelium after endothelial cell damage. The current review focuses on the role of cardiovascular risk factors on endothelial cell apoptosis and progenitor cell-mediated vasculoprotection.


Key Words: endothelial progenitor cells • risk factors • apoptosis • endothelium




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