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Review Article
Mechanisms of Disease
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Volume 352:1685-1695 April 21, 2005 Number 16
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Inflammation, Atherosclerosis, and Coronary Artery Disease
Göran K. Hansson, M.D., Ph.D.

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Recent research has shown that inflammation plays a key role in coronary artery disease (CAD) and other manifestations of atherosclerosis. Immune cells dominate early atherosclerotic lesions, their effector molecules accelerate progression of the lesions, and activation of inflammation can elicit acute coronary syndromes. This review highlights the role of inflammation in the pathogenesis of atherosclerotic CAD. It will recount the evidence that atherosclerosis, the main cause of CAD, is an inflammatory disease in which immune mechanisms interact with metabolic risk factors to initiate, propagate, and activate lesions in the arterial tree.

A decade ago, the treatment of hypercholesterolemia and hypertension . . . [Full Text of this Article]

Main Features of Atherosclerotic Lesions

Evolution of the Rupture-Prone Atherosclerotic Plaque

Gene-Targeted Mouse Models

Lipoprotein Retention and Activation of Immune Cells

            Role of Endothelial Activation, Adhesion Molecules, and Chemokines

            Macrophages in the Developing Plaque

            T-Cell Activation and Vascular Inflammation

            Antiinflammatory Factors and Disease Activity

            Cross-Talk between Inflammation and Metabolism

Infections and CAD

Acute Coronary Syndromes

Mechanisms of Plaque Rupture

Systemic Indicators of Inflammation

Inflammatory Markers and the Risk of CAD

Therapeutic Opportunities


Source Information

From the Karolinska Institute, Center for Molecular Medicine, Department of Medicine, Karolinska University Hospital, Stockholm.

Address reprint requests to Dr. Hansson at the Center for Molecular Medicine, L8:03, Karolinska University Hospital, SE-17176 Stockholm, Sweden, or at goran.hansson@cmm.ki.se.


Related Letters:

Inflammation, Atherosclerosis, and Coronary Artery Disease
García de Tena J., Kriszbacher I., Koppán M., Bódis J., Hansson G. K.
Extract | Full Text | PDF  
N Engl J Med 2005; 353:429-430, Jul 28, 2005. Correspondence

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