Fig. 3.

Metabolism of VLDL in circulation. After entering the bloodstream, VLDL undergoes hydrolysis by lipoprotein lipase (LPL), endothelial lipase, and hepatic lipase, leading to the release of free fatty acids from the core triglycerides and surface phospholipids. The activity of LPL is inhibited by apolipoprotein C3 (APOC3) and angiopoietin-like protein (ANGPTL)3/4/8, while it is activated by APOA5 and APOC2. When a large amount of triglycerides in VLDL is hydrolyzed, VLDL can be further metabolized into VLDL remnants, nearly half of which are absorbed by the liver, while the remaining VLDL remnants are further metabolized into low-density lipoprotein (LDL). LDL can bind to LDL receptors (LDLRs) and be taken up by the liver. Excessive VLDL remnants and LDL can deposit in the blood vessel walls, forming atherosclerotic plaques