Inflammation
increases
Atherosclerosis
Inflammation
increases
Atherosclerosis
6.0
ValidityScore
Valid or Invalid?
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2006
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Hansson GK, Robertson AK, Söderberg-Nauclér C -
«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 cell. Monocytes differentiate into macrophage and upregulate pattern recognition receptors, including scavenger receptors and toll-like receptors. Scavenger receptors mediate lipoprotein internalization, which lead to foam-cell formation. Toll-like receptors transmit activating signals that lead to the release of cytokines, proteases, and vasoactive molecules. T cell 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.»
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#Adaptation, Animal, Animals, Anna-Karin L Robertson, Arteries / immunology, Arteries / pathology, Atherosclerosis / drug therapy, Atherosclerosis / immunology*, Atherosclerosis / pathology*, Autoimmunity, Biomarkers, Cecilia Söderberg-Nauclér, Disease Models, Extramural, Göran K Hansson, Humans, Immunity, Immunologic Factors / therapeutic use, Inflammation / drug therapy, Inflammation / immunology*, Inflammation / pathology*, Innate, MEDLINE, N.I.H., NCBI, NIH, NLM, National Center for Biotechnology Information, National Institutes of Health, National Library of Medicine, Non-U.S. Gov', Physiological / immunology*, PubMed Abstract, Research Support, Research Support, Review, doi:10.1146/annurev.pathol.1.110304.100100, pmid:18039117, t -
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2009Publications Review
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Hansson GK -
«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 cell. Monocyte-derived macrophage 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 cell 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.»
- Organism: Humans
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#Atherosclerosis / pathology*, G K Hansson, Humans, Immune System / pathology, Inflammation / complications, Inflammation / etiology*, Inflammation / immunology, MEDLINE, NCBI, NIH, NLM, National Center for Biotechnology Information, National Institutes of Health, National Library of Medicine, Non-U.S. Gov', PubMed Abstract, Research Support, Review, doi:10.1111/j.1538-7836.2009.03416.x, pmid:19630827, t -
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on Feb 20, 2021