Excessive 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 and its active components,
polyoxygenated cholesteryl ester hydroperoxides, are involved in endogenous activation of
toll-like receptor-4 (TLR4), which in turn leads to robust cytoskeletal rearrangements and …