Key result
Review highlights VLDL biology, macrophage dynamics in atherosclerosis regression, and plaque-targeting nanoparticles.
Why the study?
Understanding the cellular mechanisms of apolipoprotein B-containing lipoprotein retention and macrophage reactions is essential for advancing atherosclerosis regression strategies.
This review summarizes the 2013 George Lyman Duff Memorial Lecture on atherogenesis, macrophage dynamics in atherosclerosis regression, and nanoparticle applications.
Supports mechanistic focus on apoB retention and macrophage responses; leaves open translation to targeted therapies pending clinical trials.
Cardinal events in atherogenesis are the retention of apolipoprotein B-containing lipoproteins in the arterial wall and the reaction of macrophages to these particles. My laboratory has been interested in both the cell biological events producing apolipoprotein B-containing lipoproteins, as well as in the reversal of the damage they cause in the plaques formed in the arterial wall. In the 2013 George Lyman Duff Memorial Lecture, as summarized in this review, I covered 3 areas of my past, present, and future interests, namely, the regulation of hepatic very low density lipoprotein production by the degradation of apolipoprotein B100, the dynamic changes in macrophages in the regression of atherosclerosis, and the application of nanoparticles to both image and treat atherosclerotic plaques.
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Edward A. Fisher (2015) conducted a review in Atherosclerosis. This review summarizes the 2013 George Lyman Duff Memorial Lecture on hepatic VLDL production, macrophage dynamics in atherosclerosis regression, and nanoparticle applications for plaques.
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