Fig. 1.

The possible mechanisms of TRLs in the process of the onset and progression of atherosclerosis. TRLs and its lypolitic products hydrolysed by LPL and CETP, containing TRL remnants (TRL-R), sd-LDL, HDL3 (HDL remodeling), oxidized free fatty acids (ox-FFA) and others, can increase the production of reactive oxygen species (ROS) and decrease nitric oxide (NO) released by endothelium and upregulate the endothelial expression of some molecules (ICAM-1, VCAM-1 and NLRP-1), which promote endothelial dysfunction. And, TRLs and its products penetrate in intima and induce inflammation contributing to monocyte activation, adhesion and migration. Meanwhile, the endometrial leukocytes can take up TG or cholesterol contents of TRL-R to form the foam cells, and then develop into core of atherosclerotic plaque. Additionally, a number of cytokines (containing TNF-α, IL-1β and others) and T cells take part in process of atherosclerosis and the whole process of atherosclerosis involves in platelet activation and aggregation to induce a procoagulant state and clot formation, in hypertriglyceridemia. Abbreviations: LPL lipoprotein lipase CETP cholesterol ester transporter proteinTRL triglyceride-rich lipoproteins TRL-R triglyceride-rich lipoprotein remnants sdLDL small and dense LDL HDL high-density lipoprotein ICAM-1 intercelluar adhesion molecule-1 VCAM-1 vascular cell adhesion molecule-1 NLRP-1 nucleotide-binding domain-like receptor family pyrin domain-containing protein 1 TNF-α tumor necrosis factor-α IL-1β interleukin-1 β