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Atherosclerosis : basic mechanisms : oxidation, inflammation, and genetics

The clinical events resulting from atherosclerosis are directly related to the oxidation of lipids in LDLs that become trapped in the extracellular matrix of the subendothelial space. These oxidized lipids activate an NF kappa B-like transcription factor and induce the expression of genes containing...

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Published in:Circulation (New York, N.Y.) N.Y.), 1995-05, Vol.91 (9), p.2488-2496
Main Authors: BERLINER, J. A, MOHAMAD NAVAB, FOGELMAN, A. M, FRANK, J. S, DEMER, L. L, EDWARDS, P. A, WATSON, A. D, LUSIS, A. J
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cited_by cdi_FETCH-LOGICAL-c391t-bd238b6d6eafc2131a89290ee5f8d8b8a262d8d1dba0dec2fe8d2f11d363f01c3
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container_issue 9
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container_title Circulation (New York, N.Y.)
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creator BERLINER, J. A
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description The clinical events resulting from atherosclerosis are directly related to the oxidation of lipids in LDLs that become trapped in the extracellular matrix of the subendothelial space. These oxidized lipids activate an NF kappa B-like transcription factor and induce the expression of genes containing NF kappa B binding sites. The protein products of these genes initiate an inflammatory response that initially leads to the development of the fatty streak. The progression of the lesion is associated with the activation of genes that induce arterial calcification, which changes the mechanical characteristics of the artery wall and predisposes to plaque rupture at sites of monocytic infiltration. Plaque rupture exposes the flowing blood to tissue factor in the lesion, and this induces thrombosis, which is the proximate cause of the clinical event. There appear to be potent genetically determined systems for preventing lipid oxidation, inactivating biologically important oxidized lipids, and/or modulating the inflammatory response to oxidized lipids that may explain the differing susceptibility of individuals and populations to the development of atherosclerosis. Enzymes associated with HDL may play an important role in protecting against lipid oxidation in the artery wall and may account in part for the inverse relation between HDL and risk for atherosclerotic clinical events.
doi_str_mv 10.1161/01.CIR.91.9.2488
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subjects Arteriosclerosis - genetics
Arteriosclerosis - physiopathology
Atherosclerosis (general aspects, experimental research)
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Humans
Inflammation
Lipoproteins - metabolism
Medical sciences
title Atherosclerosis : basic mechanisms : oxidation, inflammation, and genetics
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