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(Circulation. 2004;110:1341-1342.)
© 2004 American Heart Association, Inc.

Editorial

Targeting the Chemokines in Myocardial Inflammation

Nikolaos G. Frangogiannis, MD; Mark L. Entman, MD

From the Section of Cardiovascular Sciences, The Methodist Hospital and the DeBakey Heart Center, Baylor College of Medicine, Houston, Tex.

Correspondence and reprint requests to Nikolaos Frangogiannis, MD, Section of Cardiovascular Sciences, One Baylor Plaza M/S F-602, Baylor College of Medicine, Houston TX 77030. E-mail ngf@bcm.tmc.edu

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

The chemokines comprise a large family of small, highly basic proteins that play a critical role in basal and inflammatory leukocyte locomotion and trafficking.^1,2 In addition to effects on cell locomotion, certain chemokines are capable of eliciting a variety of other responses affecting leukocyte adhesion, activation, and degranulation, mitogenesis, and apoptosis. Furthermore, chemokines have a wide range of effects on many different cell types beyond the immune system, including endothelial cells, fibroblasts, smooth muscle cells, neurons, and epithelial cells.

See p 1443

Involvement of chemokines in the pathobiology of conditions such as multiple sclerosis, HIV disease, asthma, rheumatoid arthritis, atherosclerosis, and neoplasia has been inferred by animal model experiments and supported by correlative data in humans. Although recent investigations indicated marked chemokine upregulation in the myocardial inflammatory processes associated with infarction,^3–5 ischemic cardiomyopathy,^6,7 allograft rejection,^8,9 and myocarditis, the exact role of chemokine signaling in myocardial pathology remains poorly understood.

Chemokine induction seems to be a prominent response to myocardial injury in a variety of situations. In myocardial infarcts, cellular necrosis may trigger several chemokine-inducing pathways regulated through free radical generation, nuclear factor-B activation, tumor necrosis factor- release, and complement activation. Both CC (CCL2/monocyte chemoattractant protein-1, CCL3/macrophage inflammatory protein [MIP]-1, and CCL4/MIP-1ß) and CXC chemokines (such as CXCL10/interferon- inducible protein-10 and CXCL8/interleukin-8) are markedly induced in the infarcted myocardium.^5,4 In contrast, brief sublethal myocardial ischemia is not associated with infarction and induces chemokine upregulation mainly through reactive oxygen intermediates.¹⁰ In the ischemic myocardium, chemokine responses are robust but transient, . . . [Full Text of this Article]

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