Open AccessJournal Article
Atherosclerosis is an Inflammatory Disease
光宏 横山,Russell Ross +1 more
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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.About:
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.read more
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Parenteral iron formulations: A comparative toxicologic analysis and mechanisms of cell injury
TL;DR: In this article, the authors compared the potential of four parenteral iron formulations: Fe dextran (Fe dext), Fe sucrose (Fe sucr), Fe gluconate (Fe gluc), and Fe oligosaccharide (Fe OS).
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Vascular smooth muscle cell activation by C-reactive protein.
TL;DR: CRP causes NF-kappaB activation which could lead to the induction of MCP-1, IL-6, and iNOS gene expression and activates the MAPK-->c-Fos/cJun-->AP-1 pathway, which may play a role in atherogenesis by activating VSMC.
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Cardiovascular Function in Acromegaly
TL;DR: In this paper, the authors present evidence that effective treatment to lower serum GH levels to less than 1-2 ng/ml (glucose suppressed or random) and normalize IGF-I improves long-term outcome and survival.
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Vascular aspects of multiple sclerosis
TL;DR: Three types of vascular dysfunction have been described in multiple sclerosis (MS), and data suggest that a subtype of focal MS lesions might have an ischaemic origin, and there seems to be a link between reduced white matter perfusion and cognitive dysfunction in MS.
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Transcriptional regulatory networks in lipid metabolism control ABCA1 expression
Gerd Schmitz,Thomas Langmann +1 more
TL;DR: A highly sophisticated transcriptional network controls the balanced expression of ABCA1, and a growing list of natural and synthetic substances and metabolic regulators such as retinoids, PPAR-ligands, hormones, cytokines, and drugs are particularly effective in modulatingABCA1 and ABCG1 gene expression.
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
J. Shepherd,Stuart M. Cobbe,Ian Ford,C. G. Isles,AR Lorimer,Peter W. Macfarlane,J. H. Mckillop,Christopher J. Packard +7 more
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
Seymour Glagov,Elliot Weisenberg,Christopher K. Zarins,Regina Stankunavicius,George J. Kolettis +4 more
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.