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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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NF-kappaB, Nrf2, and HO-1 interplay in redox-regulated VCAM-1 expression.

TL;DR: Whether transcription factors known to be regulated by oxidation, i.e., the nuclear factor-κB and the Keap1/Nrf2 system, were affected in a set of cells: SMC, SMCPH GPx, and SMCLOX, as well as ECV and ECVPHGPx is investigated.
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Marine Algae-Derived Bioactive Peptides for Human Nutrition and Health

TL;DR: This review presents an overview of marine algae-derived bioactive peptides and especially highlights some key issues, such as in silico proteolysis and quantitative structure-activity relationship studies, in vivo fate of bio active peptides, and novel technologies in bioactive Peptide studies and production.
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Are there bi-directional associations between depressive symptoms and C-reactive protein in mid-life women?

TL;DR: Higher CRP levels led to higher subsequent depressive symptoms, albeit the effect was small, and the study demonstrates the importance of considering bi-directional relationships for depression and other psychosocial factors and risk for heart disease.
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Dietary pattern, inflammation and cognitive decline: The Whitehall II prospective cohort study

TL;DR: A dietary pattern characterized as higher intake of red and processed meat, peas, legumes and fried food, and lower intake of whole grains was associated with higher inflammatory markers and accelerated cognitive decline at older ages, which supports the case for further research.
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Serial contrast-enhanced cardiac magnetic resonance imaging demonstrates regression of hyperenhancement within the coronary artery wall in patients after acute myocardial infarction

TL;DR: Serial CE-CMR identified changes in spatial extent and intensity of coronary contrast enhancement in patients after acute myocardial infarction and may offer the potential for visualization of inflammatory activity in atherosclerosis associated with acute coronary syndromes.
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.