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Editorial
. 2008 Jun 20;102(12):1445-7.
doi: 10.1161/CIRCRESAHA.108.178947.

As macrophages indulge, atherosclerotic lesions bulge

Alan Daugherty, Debra L Rateri, Hong Lu
Editorial

As macrophages indulge, atherosclerotic lesions bulge

Alan Daugherty et al. Circ Res. .
No abstract available

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Figures

Figure 1
Figure 1. Lipoprotein-cholesterol ester trafficking in macrophages
Modified lipoproteins are transported into macrophages through scavenger receptors (including SR-A and CD36). In lysosomes, cholesterol esters (CE) are cleaved to unesterified cholesterol (UC) by acid cholesterol ester hydrolase (ACEH). Unesterified cholesterol is transported out of lysosomes and re-esterified by acyl CoA: cholesterol acyltransferase (ACAT) to form cholesterol esters that are stored in lipid droplets. Cholesterol esters are cleaved to cholesterol by neutral cholesterol ester hydrolase (NCEH). Unesterified cholesterol can be transferred to the extracellular space by several potential transporters (including ABCA1, ABCG1, and SR-B1) to acceptor molecules such as HDL. The lipid droplets are associated with ADFP. Paul et al. demonstrated that absence of ADFP prevented lipid engorgement, both in vitro and in vivo. The effects of macrophage-specific regulation of receptors, enzymes, and transporters on lipoprotein-cholesterol ester trafficking are denoted as: A. Absence decreases atherosclerosis. B. Absence increases atherosclerosis. C. Overexpression decreases atherosclerosis. D. Absence has inconsistent effects on atherosclerosis.
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Comment on

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