Figure 2.

Possible mechanisms of TRLs in the process of the onset and progression of atherosclerosis. Catabolism of TRL leads to the production of FFA, sdLDL and their oxidized products, oxidized FFA and ox-sdLDL and remnant particles. Catabolic products of triglycerides increase the production of ROS, increase oxidative stress, reduce NO production, induce EC apoptosis, effects insulin signalling leading to IR, vascular inflammation the expression of proinflammatory cytokines and upregulate endothelial expression adhesion molecules (ICAM-1 and VCAM-1) facilitating the migration of proinflammatory leucocytes to enhance inflammatory response (55). Retention of TRL lipoproteins, remanent particles and breakdown products in vascular intima attract monocytes that differentiate into macrophages leading to the production of foam cells after engulfing TRL and remanent particles, which form the core of atherosclerotic plaque. The proinflammatory milieu leads to aggregation and activation of platelets and coagulation cascade, thereby inducing a pro-coagulant state and clot formation (55, 56, 60). CAM, intercellular adhesion molecule; EC, endothelial cells; FFA, free fatty acid; IR, insulin resistance; ICAM, inter-cellular adhesion molecule; LPL, lipoprotein lipase; NO: nitric oxide; ox, oxidised; sdLDL, small dense LDL; TNF, Tumour necrosis factor; TRL, triglyceride rich lipoproteins; TRLR, triglyceride rich lipoprotein remnants; VCAM, vascular cell adhesion molecule.