Abstract
Key components of atherosclerotic plaque known to drive disease progression are macrophages and cholesterol. It has been widely understood, and bolstered by recent evidence, that the efflux of cholesterol from macrophage foam cells quells disease progression or even to promote regression. Following macrophage cholesterol efflux, cholesterol loaded onto HDL must be removed from the plaque environment. Here, we focus on recent evidence that the lymphatic vasculature is critical for the removal of cholesterol, likely as a component of HDL, from tissues including skin and the artery wall. We discuss the possibility that progression of atherosclerosis might in part be linked to sluggish removal of cholesterol from the plaque.