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CD36/FattyAcidTranslocase,AnInflammatoryMediator,Is InvolvedinHyperlipidemia-InducedExacerbationin IschemicBrainInjury

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The article was published on 2008-01-01 and is currently open access. It has received 0 citations till now. The article focuses on the topics: CD36.

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Journal ArticleDOI

The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions

TL;DR: This work identifies two distinct phases of monocyte participation after MI and proposes a model that reconciles the divergent properties of these cells in healing and identifies new therapeutic targets that can influence healing and ventricular remodeling after MI.
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ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree.

TL;DR: The apoE-deficient mouse contains the entire spectrum of lesions observed during atherogenesis and is the first mouse model to develop lesions similar to those in humans.
Journal ArticleDOI

Inflammation as a cardiovascular risk factor.

TL;DR: In randomized, controlled trials, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, in the form of statins, have been shown to provide effective therapy for lowering CRP, in conjunction with their lipid-lowering effects.
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CD36: a class B scavenger receptor involved in angiogenesis, atherosclerosis, inflammation, and lipid metabolism

TL;DR: The biology of CD36 can be broadly divided in terms of functions that it mediates with or without TSP-1, but it is probable that it acts in concert with other proteins, such as fatty acid–binding proteins, caveola-associated proteins, integrins, cytoskeletal proteins, and signaling molecules, to effect its diverse functions.
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Targeted disruption of the class B scavenger receptor CD36 protects against atherosclerotic lesion development in mice

TL;DR: Results support a major role for CD36 in atherosclerotic lesion development in vivo and suggest that blockade of CD36 can be protective even in more extreme proatherogenic circumstances.