The effects of second-hand smoke on biological processes important in atherogenesis

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Abstract

Background
Atherosclerosis is an inflammatory disease that accounts for nearly 50% of deaths in western societies,1 Initiation of atherosclerotic plaque formation is a complex process. It involves secretion of chemokines such as the Monocyte Chemoattractant Protein├óÔé¼ÔÇ£1 (MCP-1)1-4 and expression of adhesion molecules on the surface of monocytes and endothelial cells.5-7 Circulating monocytes are recruited to sites of injured endothelial cells, adhere to them, and migrate into the subendothelial space. Monocytes in the arterial wall differentiate into activated macrophages that are efficient scavengers of oxidized low density lipoprotein (LDL). When exposed to large amounts of oxidized LDL, these macrophages accumulate large amounts of cholesteryl esters in lipid droplets and become \foam cells\" that form \"fatty streaks\", the precursors of more complicated atherosclerotic plaques.8,9

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