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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board Member: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Sies, Helmut / Turk, Boris / Wittinghofer, Alfred


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1437-4315
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Adult progenitor cells in vascular remodeling during atherosclerosis

Mihail Hristov1 / Alma Zernecke2 / Andreas Schober3 / Christian Weber4

1Institut für Molekulare Herz-Kreislaufforschung (IMCAR), Universitätsklinikum der RWTH Aachen, Pauwelsstrasse 30, D-52074 Aachen, Germany and IZKF ‘BIOMAT’, Universitätsklinikum der RWTH Aachen, Pauwelsstrasse 30, D-52074 Aachen, Germany

2Institut für Molekulare Herz-Kreislaufforschung (IMCAR), Universitätsklinikum der RWTH Aachen, Pauwelsstrasse 30, D-52074 Aachen, Germany

3Abteilung Kardiologie, Medizinische Poliklinik, Klinikum der LMU München, Pettenkoferstrasse 8a, D-80336 München, Germany

4Institut für Molekulare Herz-Kreislaufforschung (IMCAR), Universitätsklinikum der RWTH Aachen, Pauwelsstrasse 30, D-52074 Aachen, Germany

Corresponding author

Citation Information: Biological Chemistry. Volume 389, Issue 7, Pages 837–844, ISSN (Online) 1437-4315, ISSN (Print) 1431-6730, DOI: 10.1515/BC.2008.093, June 2008

Publication History

Published Online:
2008-06-06

Abstract

The mobilization and recruitment of bone marrow-derived, circulating or tissue resident progenitor cells giving rise to smooth muscle-like cells have been implicated in neointima hyperplasia after arterial injury and in accelerated forms of arterial lesion formation, e.g., transplant arteriopathy or graft vasculopathy. By contrast, convincing evidence has emerged that the vascular homing of endothelial progenitor cells (EPCs) contributes to endothelial recovery, thus limiting neointima formation after arterial injury. In the chronic context of primary atherosclerosis, plaque progression and destabilization, a more complex picture has become apparent. In patients with coronary artery disease, the number and function of EPCs have been linked with an improved endothelial function or regeneration, but have been inversely correlated with cardiovascular risk. In animal models, however, the injection of bone marrow cells or EPCs, or the application of stem-cell mobilizing factors, have been associated with an exacerbation of atherosclerosis and unstable plaque phenotypes, whereas the contribution of bone marrow-derived smooth muscle progenitors to primary atherosclerosis appears to be rather confined. Here, we discuss crucial biochemical cues, namelychemokines, adhesion molecules, growth factors and pharmacological means that guide and control the context-specific mobilization, recruitment and fate of vascular progenitor cells in arterial remodeling during atherosclerosis.

Keywords: arterial disease; chemokines; myocardial infarction; stem cells

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