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J Thromb Haemost. 2009 Jul;7 Suppl 1:328-31. doi: 10.1111/j.1538-7836.2009.03416.x.

Inflammatory mechanisms in atherosclerosis.

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1
Karolinska Institutet, Center for Molecular Medicine L8:03, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden. Goran.Hansson@ki.se

Abstract

Atherosclerosis, the cause of myocardial infarction, stroke and ischemic gangrene, is an inflammatory disease. When LDL accumulates in the intima, it activates the endothelium to express leukocyte adhesion molecules and chemokines that promote recruitment of monocytes and T cells. Monocyte-derived macrophages upregulate pattern recognition receptors, including scavenger receptors that mediate uptake of modified LDL, and Toll-like receptors, which transmit activating signals leading to release of cytokines, proteases, and vasoactive molecules. T cells in lesions recognize local antigens and mount Th1 responses with secretion of pro-inflammatory cytokines, thus contributing to local inflammation and growth of the plaque. Intensified inflammatory activation may lead to local proteolysis, plaque rupture, and thrombus formation, triggering ischemia and infarction. Inflammatory markers are already used to monitor the disease process and anti-inflammatory therapy may be useful to control disease activity.

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