HDLs protect against the development of atherosclerosis, but the underlying mechanisms
are poorly understood. HDL and its apolipoproteins can promote cholesterol efflux from …

Rationale: Macrophages cannot limit the uptake of lipids and rely on cholesterol efflux
mechanisms for maintaining cellular cholesterol homeostasis. Important mediators of …

With the aim of identifying new target genes that could contribute to limit foam cell formation,
we analyzed changes in the pattern of gene expression in human THP-1 macrophages …

Macrophage uptake of oxidized low-density lipoprotein (oxLDL) is thought to play a central
role in foam cell formation and the pathogenesis of atherosclerosis. We demonstrate here …

Accumulation of macrophage foam cells in atherosclerotic blood vessel intima is a critical
component of atherogenesis mediated by scavenger receptor-dependent internalization of …

Cholesteryl ester accumulation by macrophages is a critical early event in atherogenesis. To
test the hypothesis that sterol loading promotes foam cell formation and vascular disease by …

Atherogenesis requires and is highly influenced by the interaction between lipoproteins and
macrophages. Most of the focus to date has been on the ability of atherogenic lipoproteins …

Previously, we reported that fluid-phase endocytosis of native LDL by PMA-activated human
monocytederived macrophages converted these macrophages into cholesterol-enriched …

The concept that macrophages can become foam cells as a result of a disturbed balance
between the uptake of cholesterol from lipoproteins and cholesterol efflux is generally …

Macrophages are key to the pathogenesis of atherosclerosis. They take up and store
excessive amounts of cholesterol associated with modified low density lipoprotein …