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Experimental Atherosclerosis Section

Howard Kruth, MD, Principal Investigator

Microscopic view of  human atherosclerotic plaque. Cholesteryl ester is labeled red, unesterified cholesterol is labeled green.  Arrows show cholesteryl ester-rich foam cells.
Microscopic view of  human atherosclerotic plaque.

Our research program is directed towards understanding the mechanisms by which cholesterol accumulates within arteries causing atherosclerotic plaques to form, the cause of most heart attacks and strokes. We are investigating endocytic pathways by which endothelial cells transport LDL, cholesterol-carrying lipoproteins, into the vessel wall, and by which macrophages within the vessel wall then take up these LDL. Both processes contribute to atherosclerotic plaque development. Biochemical, cell biological, and molecular biological studies of LDL processing by these cells in culture are being carried out. Our studies have led to the discovery of a novel mechanism by which macrophages accumulate cholesterol and transform into plaque-generating foam cells. Activated macrophages take up LDL in the fluid-phase by receptor-independent pinocytosis of LDL. Elucidation of the signaling pathways that mediate macrophage pinocytosis of LDL will provide new drug targets with the potential to limit plaque cholesterol accumulation.

 

 

 

 

 


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Department of Health and Human Services National Institutes of Health National Heart, Lung, and Blood Institute