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lüll Toll-like receptor-4 and lipoprotein accumulation in macrophages Miller YI; Choi SH; Fang L; Harkewicz RTrends Cardiovasc Med 2009[Oct]; 19 (7): 227-32Excessive lipid accumulation in macrophages, also known as foam cell formation, is a key process during the development of atherosclerosis, leading to vascular inflammation and plaque growth. Recent studies have identified a new mechanism of macrophage lipid accumulation in which minimally oxidized low-density lipoprotein (mmLDL) and its active components, polyoxygenated cholesteryl ester hydroperoxides, are involved in endogenous activation of toll-like receptor-4 (TLR4), leading to recruitment of spleen tyrosine kinase (Syk), robust cytoskeletal rearrangements and macropinocytosis. In hyperlipidemic environments, mmLDL-induced, TLR4- and Syk-dependent macropinocytosis leads to substantial lipid accumulation in macrophages and monocytes, which may constitute an important mechanism of foam cell formation in atherosclerosis. A novel hypercholesterolemic zebrafish model of early stages of atherosclerosis was used to demonstrate that the TLR4 deficiency significantly reduces the in vivo rate of macrophage lipid accumulation in vascular lesions.|Animals[MESH]|Atherosclerosis/pathology[MESH]|Cholesterol Esters/metabolism[MESH]|Foam Cells/*metabolism/pathology[MESH]|Humans[MESH]|Lipoproteins, LDL/*metabolism/physiology[MESH]|Macrophages/cytology/*metabolism/physiology[MESH]|Models, Biological[MESH]|Toll-Like Receptor 4/*metabolism[MESH]|Zebrafish[MESH] |