Our previous studies demonstrated that nicotine, the major chemical of cigarette smoke, induced insulin resistance and the formation of abdominal aortic aneurysm in mice in vivo.27, 28 Also, cigarette smoke was reported to contribute to atherosclerosis, in which some mechanisms were revealed.29 For instance, nicotine was related to induced thrombosis, dyslipidemia and vascular inflammation.30, 31 In this study, we found that nicotine suppressed HuR translocation, which resulted in reduced GTPCH1 level and endothelial dysfunction. This evidence concerns the gene ELAVL1 and metabolic syndrome.