Macrophage cholesteryl ester mobilization and atherosclerosis
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TLDR
In this article, the authors summarize the earlier controversies surrounding the identity of neutral cholesteryl ester hydrolase (CEH) in macrophages, discuss the characteristics of various candidates recognized to date and examine their role in mobilizing cellular CE and thus regulating atherogenesis and emphasize the importance of evaluating the biochemical characteristics of candidate enzymes that may be targeted in the future to attenuate atherosclerosis.About:
This article is published in Vascular Pharmacology.The article was published on 2010-01-01 and is currently open access. It has received 129 citations till now. The article focuses on the topics: Cholesteryl ester & Sterol O-acyltransferase.read more
Citations
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Journal ArticleDOI
The biophysics and cell biology of lipid droplets
TL;DR: The regulation of the composition of the phospholipid surfactants at the surface of lipid droplets is crucial for lipid droplet homeostasis and protein targeting to their surfaces.
Journal ArticleDOI
Autophagy Regulates Cholesterol Efflux from Macrophage Foam Cells via Lysosomal Acid Lipase
TL;DR: It is concluded that, in macrophage foam cells, lysosomal hydrolysis contributes to the mobilization of LD-associated cholesterol for reverse cholesterol transport.
Journal ArticleDOI
Foam cells in atherosclerosis.
TL;DR: What is known about the mechanisms of cholesterol uptake, esterification and release in macrophages is described to help develop novel therapeutic interventions for atherosclerosis.
Journal ArticleDOI
Regulation of lipid stores and metabolism by lipophagy
K Liu,Mark J. Czaja +1 more
TL;DR: The ability of the cell to alter the amount of lipid targeted for autophagic degradation depending on nutritional status demonstrates that this process is selective.
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Macrophage-mediated cholesterol handling in atherosclerosis.
Dimitry A. Chistiakov,Yuri V. Bobryshev,Yuri V. Bobryshev,Alexander N. Orekhov,Alexander N. Orekhov +4 more
TL;DR: In atherosclerosis, disruption of lipid homoeostasis in macrophages leads to cholesterol accumulation and formation of foam cells, a hallmark at the initial stages of Atherosclerosis.
References
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Journal ArticleDOI
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.
Journal ArticleDOI
Atherosclerosis: The Road Ahead
TL;DR: Elevated levels of serum cholesterol are probably unique through the hepatic LDL receptor pathway, as evi-in being sufficient to drive the development of athero-denced by the fact that lack of functional LDL receptors sclerosis in humans and experimental animals, even in is responsible for the massive accumulation of LDL in the absence of other known risk factors.
Journal ArticleDOI
Plaque fissuring--the cause of acute myocardial infarction, sudden ischaemic death, and crescendo angina.
M J Davies,A C Thomas +1 more
TL;DR: This controversy was concerned with whether coronary artery thrombi were or were not directly responsible for all three clinical pictures of acute ischaemia.
Journal ArticleDOI
Effect of recombinant ApoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes: a randomized controlled trial.
Steven E. Nissen,Taro Tsunoda,E. Murat Tuzcu,Paul Schoenhagen,Christopher J. Cooper,Muhammad Yasin,Gregory M. Eaton,Michael A Lauer,W. Scott Sheldon,Cindy L. Grines,Stephen H. Halpern,Tim Crowe,James C. Blankenship,Richard A. Kerensky +13 more
TL;DR: A recombinant ApoA-I Milano/phospholipid complex administered intravenously for 5 doses at weekly intervals produced significant regression of coronary atherosclerosis as measured by IVUS, and results require confirmation in larger clinical trials with morbidity and mortality end points.
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The Response-to-Retention Hypothesis of Early Atherogenesis
Kevin Jon Williams,Ira Tabas +1 more
TL;DR: Subendothelial retention of atherogenic lipoproteins as the central pathogenic process in atherogenesis is strongly supported, and other contributory processes are either not individually necessary or are not sufficient.