Figure 3. Impact of various sorting nexins (SNXs) on the etiology and sequelae of cardiovascular disease.

Several SNXs have been identified to impinge on some of the well-known underlying mechanisms, complications, and utility for pharmacogenomics for cardiovascular disease. Arrows (↑ or ↓) indicate the pathological change in the expression or activity of SNXs in the respective disease, and the corresponding change of their targets (receptor/enzyme/transporter/inflammatory cytokines) is also in brackets, either activation (in blue), inactivation (in red), or unknown (in green). rs28891 is a SNP of SNX24 that predispose to the development of coronary artery aneurysm. The PDZ domain of SNX27 is essential for PDZ-directed recycling of the β₂AR, apolipoprotein E receptor 2 (ApoER2), apoptosis repressor with caspase recruitment domain (ARC), β₁-adrenergic receptor blocker (β₁-blocker), β₂-adrenergic receptor blocker (β₂-blocker), dense core vesicles (DCVs), dopamine D₁ receptor (D₁R); dopamine D₂ receptor (D₂R); dopamine D₅ receptor (D₅R), epithelial sodium channel (ENaC), glucagon-like peptide-1 receptor (GLP-1R), glucose transporter 1 (GLUT1) or 4 (GLUT4), insulin degrading enzyme (IDE), insulin receptor (IR), interleukin (IL), leptin receptor (OB-R), low density lipoprotein receptor (LDL-R), LDL-R-related protein (LRP), protease-activated receptor (PAR1), sarcoplasmic reticulum Ca²⁺-ATPase2a (SERCA2a), sodium hydrogen exchanger type 3 (NHE3), sorting nexin (SNX).