STAT3 and atherosclerosis: The exacerbation of atherosclerosis produced by TMAO includes a positive feedback loop generated by the up-regulation of lncRNA enriched abundant transcript 1 (NEAT1), a regulator of endothelial cell behavior, and miR-370-3p/signal transducer and activator of transcription 3 (STAT3)/flavin-containing monooxygenase-3 axis (FMO3), a cascade that produces excessive proliferation and decreased apoptosis of human aortic endothelial cells [141].