Journal of Leukocyte Biology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published online as doi:10.1189/jlb.1206761 on March 29, 2007

Published online before print March 29, 2007
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jlb.1206761v1
82/2/226    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Barlic, J.
Right arrow Articles by Murphy, P. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barlic, J.
Right arrow Articles by Murphy, P. M.
(Journal of Leukocyte Biology. 2007;82:226-236.)
© 2007 by Society for Leukocyte Biology

Chemokine regulation of atherosclerosis

Jana Barlic and Philip M. Murphy1

Molecular Signaling Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA

1 Correspondence: NIH, NIAID, Bldg. 10, Rm. 11N113, Bethesda, MD 20892, USA. E-mail: pmm{at}nih.gov

ABSTRACT

Oxidative stress and inflammation are accepted as major factors in the pathogenesis of atherosclerosis, but how they interact to produce a plaque has not been delineated clearly. Recent data suggest that oxidized lipids may act in part by regulating production of chemokines and chemokine receptors, which in turn, may direct monocytes and other blood leukocytes to the vessel wall, where they may interact with endothelial cells and smooth muscle cells. The receptors may act at the level of recruitment, retention, and egress, not only through classic, chemotactic mechanisms but also through direct, intercellular adhesion. The results suggest a coordinated mechanism for inflammatory cell accumulation in plaque and identify novel targets, such as CCR2 and CX3CR1, for potential drug development in coronary artery disease.

Key Words: leukocytes • atherogenesis




This article has been cited by other articles:


Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
P. Aukrust, B. Halvorsen, A. Yndestad, T. Ueland, E. Oie, K. Otterdal, L. Gullestad, and J. K. Damas
Chemokines and Cardiovascular Risk
Arterioscler. Thromb. Vasc. Biol., November 1, 2008; 28(11): 1909 - 1919.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2007 by the Society for Leukocyte Biology.