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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.
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.

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Citations
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n-3 Fatty acids and cardiovascular disease: evidence explained and mechanisms explored.

TL;DR: A recent study suggests that long-chain n-3 PUFAs might also act to stabilize advanced atherosclerotic plaques, perhaps through their anti-inflammatory effects.
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Vascular Inflammation and the Renin-Angiotensin System

TL;DR: A molecular mechanism for a biological positive-feedback loop that explains how vascular inflammation can be self-sustaining through upregulation of the vessel wall Ang II tone is defined, suggesting that one mechanism by which RAS antagonists prevent atherosclerosis is by reducing vascular inflammation.
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Cardiovascular disease and chronic renal disease: a new paradigm.

TL;DR: A paradigm that CVD and CRD are outcomes of the same underlying disorders is proposed, and risk factor reduction strategies used to prevent CVD in the general population also be applied to patients with CRD, with the hope of preventing progression of renal disease, as well as preventing CVD.
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Platelet Glycoprotein Ibα Is a Counterreceptor for the Leukocyte Integrin Mac-1 (Cd11b/Cd18)

TL;DR: The platelet counterreceptor is identified as glycoprotein (GP) Ibα, a component of the GP Ib-IX-V complex, the platelet von Willebrand factor (vWf) receptor, which provides a molecular target for disrupting leukocyte–platelet complexes that promote vascular inflammation in thrombosis, atherosclerosis, and angioplasty-related restenosis.
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Pregnancy-Associated Plasma Protein A as a Marker of Acute Coronary Syndromes

TL;DR: PAPP-A is present in unstable plaques, and circulating levels are elevated in acute coronary syndromes; these increased levels may reflect the instability of atherosclerotic plaques.
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.