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Inflammation and atherosclerosis.
Annu Rev Pathol. 2006; 1:297-329.AR

Abstract

Atherosclerosis, the cause of myocardial infarction, stroke, and ischemic gangrene, is an inflammatory disease. The atherosclerotic process is initiated when cholesterol-containing low-density lipoproteins accumulate in the intima and activate the endothelium. Leukocyte adhesion molecules and chemokines promote recruitment of monocytes and T cells. Monocytes differentiate into macrophages and upregulate pattern recognition receptors, including scavenger receptors and toll-like receptors. Scavenger receptors mediate lipoprotein internalization, which leads to foam-cell formation. Toll-like receptors transmit activating signals that lead to the release of cytokines, proteases, and vasoactive molecules. T cells in lesions recognize local antigens and mount T helper-1 responses with secretion of pro-inflammatory cytokines that contribute to local inflammation and growth of the plaque. Intensified inflammatory activation may lead to local proteolysis, plaque rupture, and thrombus formation, which causes 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

Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Stockholm SE-17176, Sweden. Goran.Hansson@ki.seNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

18039117

Citation

Hansson, Göran K., et al. "Inflammation and Atherosclerosis." Annual Review of Pathology, vol. 1, 2006, pp. 297-329.
Hansson GK, Robertson AK, Söderberg-Nauclér C. Inflammation and atherosclerosis. Annu Rev Pathol. 2006;1:297-329.
Hansson, G. K., Robertson, A. K., & Söderberg-Nauclér, C. (2006). Inflammation and atherosclerosis. Annual Review of Pathology, 1, 297-329.
Hansson GK, Robertson AK, Söderberg-Nauclér C. Inflammation and Atherosclerosis. Annu Rev Pathol. 2006;1:297-329. PubMed PMID: 18039117.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inflammation and atherosclerosis. AU - Hansson,Göran K, AU - Robertson,Anna-Karin L, AU - Söderberg-Nauclér,Cecilia, PY - 2007/11/28/pubmed PY - 2007/12/14/medline PY - 2007/11/28/entrez SP - 297 EP - 329 JF - Annual review of pathology JO - Annu Rev Pathol VL - 1 N2 - Atherosclerosis, the cause of myocardial infarction, stroke, and ischemic gangrene, is an inflammatory disease. The atherosclerotic process is initiated when cholesterol-containing low-density lipoproteins accumulate in the intima and activate the endothelium. Leukocyte adhesion molecules and chemokines promote recruitment of monocytes and T cells. Monocytes differentiate into macrophages and upregulate pattern recognition receptors, including scavenger receptors and toll-like receptors. Scavenger receptors mediate lipoprotein internalization, which leads to foam-cell formation. Toll-like receptors transmit activating signals that lead to the release of cytokines, proteases, and vasoactive molecules. T cells in lesions recognize local antigens and mount T helper-1 responses with secretion of pro-inflammatory cytokines that contribute to local inflammation and growth of the plaque. Intensified inflammatory activation may lead to local proteolysis, plaque rupture, and thrombus formation, which causes 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 - 1553-4006 UR - https://www.unboundmedicine.com/medline/citation/18039117/Inflammation_and_atherosclerosis_ L2 - http://arjournals.annualreviews.org/doi/full/10.1146/annurev.pathol.1.110304.100100?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -