Low-density lipoprotein (LDL) particles are known as atherogenic agents in coronary artery diseases. They modify to other electronegative forms and may be the subject for improvement of inflammatory events in vessel subendothelial spaces. The circulating LDL value is associated with the plasma PCSK-9 level. They internalize into macrophages using the lysosomal receptor-mediated pathways. LDL uptake is related to the membrane scavenger receptors, modifications of lipid and protein components of LDL particles, vesicular maturation and lipid stores of cells. Furthermore, LDL vesicular trafficking is involved with the function of some proteins such as Rab and Lamp families. These proteins also help in the transportation of free cholesterol from lysosome into the cytosol. The aggregation of lipids in the cytosol is a starting point for the formation of foam cells so that they may participate in the primary core of atherosclerosis plaques. The effects of macrophage subclasses are different in the formation and remodeling of plaques. This review is focused on the cellular and molecular events involved in cholesterol homeostasis.
Keywords: LDL; atherosclerosis; cholesterol; lipid droplet; lipoprotein; macrophage.