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Inflammatory mechanisms in atherosclerosis.
J Thromb Haemost. 2009 Jul; 7 Suppl 1:328-31.JT

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.

Authors+Show Affiliations

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

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

19630827

Citation

Hansson, G K.. "Inflammatory Mechanisms in Atherosclerosis." Journal of Thrombosis and Haemostasis : JTH, vol. 7 Suppl 1, 2009, pp. 328-31.
Hansson GK. Inflammatory mechanisms in atherosclerosis. J Thromb Haemost. 2009;7 Suppl 1:328-31.
Hansson, G. K. (2009). Inflammatory mechanisms in atherosclerosis. Journal of Thrombosis and Haemostasis : JTH, 7 Suppl 1, 328-31. https://doi.org/10.1111/j.1538-7836.2009.03416.x
Hansson GK. Inflammatory Mechanisms in Atherosclerosis. J Thromb Haemost. 2009;7 Suppl 1:328-31. PubMed PMID: 19630827.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inflammatory mechanisms in atherosclerosis. A1 - Hansson,G K, PY - 2009/7/28/entrez PY - 2009/7/28/pubmed PY - 2009/12/16/medline SP - 328 EP - 31 JF - Journal of thrombosis and haemostasis : JTH JO - J. Thromb. Haemost. VL - 7 Suppl 1 N2 - 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. SN - 1538-7836 UR - https://www.unboundmedicine.com/medline/citation/19630827/Inflammatory_mechanisms_in_atherosclerosis_ L2 - https://doi.org/10.1111/j.1538-7836.2009.03416.x DB - PRIME DP - Unbound Medicine ER -
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