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0 reviewsSUMMARYDietary fat drives the pathogenesis of atherosclerotic cardiovascular disease (ASCVD), particularly throughcirculating cholesterol and triglyceride-rich lipoprotein remnants. Industrially produced trans-unsaturatedfatty acids (TFAs) incorporated into food supplies significantly promote ASCVD. However, the molecular trafficking of TFAs responsible for this association is not well understood. Here, we demonstrate that TFAs arepreferentially incorporated into sphingolipids by serine palmitoyltransferase (SPT) and secreted from cellsin vitro. Administering high-fat diets (HFDs) enriched in TFAs to Ldlr/ mice accelerated hepatic very-lowdensity lipoprotein (VLDL) and sphingolipid secretion into circulation to promote atherogenesis comparedwith a cis-unsaturated fatty acid (CFA)-enriched HFD. SPT inhibition mitigated these phenotypes andreduced circulating atherogenic VLDL enriched in TFA-derived polyunsaturated sphingomyelin. Transcriptional analysis of human liver revealed distinct regulation of SPTLC2 versus SPTLC3 subunit expression,consistent with human genetic correlations in ASCVD, further establishing sphingolipid metabolism as a critical node mediating the progression of ASCVD in response to specific dietary fats.