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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Non-steroidal anti-inflammatory drugs and risk of serious coronary heart disease: an observational cohort study ☆
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High-sensitivity C-reactive protein in high-grade carotid stenosis: risk marker for unstable carotid plaque ☆
TL;DR: Assessment of circulating hs-CRP levels may be a useful additional marker of risk in patients with high-grade carotid stenosis and may be related to the presence of macrophages and T lymphocytes in plaque, which is associated with the phenomena of instability that can lead to development of an ischemic event.
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Fibrillar Amyloid Protein Present in Atheroma Activates CD36 Signal Transduction
Lea A. Medeiros,Tayeba Khan,Joseph El Khoury,Chi L.L. Pham,Danny M. Hatters,Geoffrey J. Howlett,Roland Lopez,Kevin D. O'Brien,Kathryn J. Moore +8 more
TL;DR: This work shows that apolipoprotein C-II, a component of very low and high density lipoproteins, readily forms amyloid fibrils that initiate macrophage inflammatory responses including reactive oxygen production and tumor necrosis factor α expression, and characterize a CD36-dependent signaling cascade initiated by fibrillar amyloids species that may promote atherogenesis.
Journal ArticleDOI
Obstructive Sleep Apnea and Inflammation
TL;DR: The precise role of inflammation in the development of cardiovascular disease in OSAS requires further study, particularly the relationship with oxidative stress, metabolic dysfunction, and obesity.
BookDOI
Fundamentals of Inflammation
TL;DR: The text is presented as an introductory springboard for graduate students, postdoctoral Fellows, medical scientists, and researchers from other disciplines who wish to gain an appreciation and working knowledge of current cellular and molecular mechanisms fundamental to inflammation.
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.