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Open AccessJournal Article

Atherosclerosis is an Inflammatory Disease

光宏 横山, +1 more
- 28 Feb 1998 - 
- Vol. 62, pp 8
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TLDR
Despite changes in lifestyle and the use of new pharmacologic approaches to lower plasma cholesterol concentrations, cardiovascular disease continues to be the principal cause of death in the United States, Europe, and much of Asia.
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This article is published in Japanese Circulation Journal-english Edition.The article was published on 1998-02-28 and is currently open access. It has received 9749 citations till now. The article focuses on the topics: Disease.

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Citations
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Increased level of advanced oxidation protein products in patients with coronary artery disease.

TL;DR: Multivariable regression models revealed that the plasma AOPP level was significantly related to CAD status, the first report of an association between AOPp and CAD.
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PPARα in atherosclerosis and inflammation

TL;DR: Evidence suggests activation of PPARα inhibits the formation of macrophage foam cells by regulating expression of genes involved in reverse cholesterol transport, formation of reactive oxygen species (ROS), and associated lipoprotein oxidative modification among others, and PPAR α may increase the stability of atherosclerotic plaques and limit plaque thrombogenicity.
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Inflammatory cytokines, socioeconomic status, and acute stress responsivity

TL;DR: Plasma concentrations at rest of TNF-alpha, IL-1Ra, and IL-6 (women only) were associated with socioeconomic status, with lower levels in the high status group, but the effect was non-linear.
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Evolution of phenolic compounds from color and flavor problems to health benefits.

TL;DR: There is limited clinical evidence that certain polyphenolic metabolites by virtue of their anti-inflammatory activities can improve insulin sensitivity and endothelial and mitochondrial function, suggesting that polyphenols are good for disease prevention.
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Oxidative modification of low-density lipoprotein and immune regulation of atherosclerosis

TL;DR: Recent progress is reviewed in understanding of the mechanisms involved in oxidation of LDL, formation of oxLDL complexes, and antibody mediated-immune regulation of atherogenesis.
References
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The pathogenesis of atherosclerosis: a perspective for the 1990s

TL;DR: The ability to control the expression of genes encoding these molecules and to target specific cell types provides opportunities to develop new diagnostic and therapeutic agents to induce the regression of the lesions and, possibly, to prevent their formation.
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Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group

TL;DR: Treatment with pravastatin significantly reduced the incidence of myocardial infarction and death from cardiovascular causes without adversely affecting the risk of death from noncardiovascular causes in men with moderate hypercholesterolemia and no history of my Cardiac Infarction.
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Inflammation, Aspirin, and the Risk of Cardiovascular Disease in Apparently Healthy Men

TL;DR: The reduction associated with the use of aspirin in the risk of a first myocardial infarction appears to be directly related to the level of C-reactive protein, raising the possibility that antiinflammatory agents may have clinical benefits in preventing cardiovascular disease.
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The Pathogenesis of Atherosclerosis — An Update

TL;DR: A response-to-injury hypothesis of atherogenesis proposes that "injury" to the endothelium is the initiating event in atherosclerosis, and intimal smooth-muscle proliferation as the key event in the development of the advanced lesions of Atherosclerosis.
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Compensatory Enlargement of Human Atherosclerotic Coronary Arteries

TL;DR: It is concluded that human coronary arteries enlarge in relation to plaque area and that functionally important lumen stenosis may be delayed until the lesion occupies 40 percent of the internal elastic lamina area.