Table 1 Association of key metabolites and enzymes in sphingolipid metabolism with endothelial function, lipid lamination, and inflammatory responses during atherosclerosis

CER

Increased ROS production

Formation of LDL aggregates

Promotion of MMP-7 secretion

Reduction of NO production by PP2A

Promotion of LDL oxidation

Induction of IL-6, IL-10, and MCP-1 release

Release of granulosa cytochrome C or activation of caspase-8 promotes endothelial cell apoptosis

SM

Retention of cholesterol in cells and artery walls

Subendothelial aggregation and retention of atherogenic lipoproteins

S1P

Binding to S1PR affects endothelial cell integrity

biased distribution on HDL

Elevated local S1P levels can cause increased levels of endothelial adhesion molecules

Attenuating endothelial cell injury by activating the AKT/eNOS signaling pathway

Levels are influenced by the metabolism of ApoM lipoproteins

Recruitment of inflammatory cells

Damage to the endothelial barrier (high glucose and high concentration conditions)

Activation of dendritic cells

GSL

Promoting cellular phagocytosis of endothelial cells

Accumulation with Ox-LDL in fatty streaks and endothelial plaques

Accumulates in the vascular endothelium and promotes thrombosis

SPT

Regulation of vascular endothelial function and proliferation

Regulation of cholesterol efflux

Regulation of the inflammatory response in macrophages

SMS

Promoting endothelial dysfunction by activating the Wnt/β-catenin signaling pathway

Regulation of macrophage phagocytosis of lipids to form foam cells

Targeting SM levels on macrophage membranes and lipid rafts to regulate the NF-kappaB pathway

Upregulation of inflammatory biomarker expression

SphK

Involvement in ABCA1-mediated regulation of cholesterol efflux

Promotes vascular inflammation

Maintenance of autophagic degradation of lipid droplets in macrophages

Promotes expression of endothelial cell adhesion molecules