TLR4 and endothelial dysfunction: Furthermore, RC-derived free fatty acids (FFA) and monoacylglycerols—by-products of lipoprotein lipase (LPL) hydrolysis—activate Toll-like receptor 4 (TLR4) on endothelial cells, inducing NF-κB–mediated transcription of adhesion molecules (VCAM-1, ICAM-1) and proinflammatory cytokines (IL-1β, IL-6, TNF-α), thereby mirroring the endothelial dysfunction seen in oxidized LDL-C–mediated eNOS uncoupling (53–55).