title: A polymorphism in the visfatin gene promoter is related to decreased plasma levels of inflammatory markers in patients with coronary artery disease.
abstract: Visfatin, a newly identified proinflammatory adipokine, has been linked to coronary artery disease (CAD). The -1535C>T polymorphism (rs61330082) located in the visfatin gene promoter is reportedly associated with proinflammatory status. However, it is unclear whether this polymorphism correlates with plasma levels of inflammatory markers including visfatin, hs-CRP, IL-6 and TNF-α in CAD patients. The present study was to investigate the potential association of the -1535C>T polymorphism with plasma levels of visfatin, IL-6, C reactive protein (hs-CRP) and TNF-α in patients with CAD. We conducted a hospital based study with 171 CAD patients to examine the association between the -1535C>T polymorphism and plasma levels of visfatin, hs-CRP, IL-6 and TNF-α. Plasma visfatin levels were markedly different between patients with stable angina pectoris (SAP, 11.91 ± 0.70 ng/l) and those with unstable angina pectoris (UAP, 17.49 ± 0.20 ng/l) or acute myocardial infarction (AMI, 16.63 ± 0.22 ng/l; SAP versus UAP or AMI, P < 0.05). Compared with the CC genotype, variant genotypes CT and TT correlated with significantly lower levels of visfatin, hs-CRP, IL-6 and TNF-α in the SAP group (P < 0.05), with lower levels of hs-CRP and IL-6 in the UAP group (P < 0.05), and with lower levels of visfatin in the AMI group (P < 0.05) after adjustment for age, gender, smoking, hypertension, diabetes, dyslipidemia and medication. Our results suggest that the -1535C>T polymorphism is associated with decreased plasma levels of inflammatory markers in CAD patients, reflecting that this polymorphism might provide a useful marker for predicting the development of CAD events.
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China. drlswang@njmu.edu.cn
authors.forename: Lian-Sheng
authors.initials: LS
authors.lastname: Wang
authors.forename: Jian-Jun
authors.initials: JJ
authors.lastname: Yan
authors.forename: Na-Ping
authors.initials: NP
authors.lastname: Tang
authors.forename: Jun
authors.initials: J
authors.lastname: Zhu
authors.forename: Yue-Song
authors.initials: YS
authors.lastname: Wang
authors.forename: Qi-Ming
authors.initials: QM
authors.lastname: Wang
authors.forename: Jian-Jin
authors.initials: JJ
authors.lastname: Tang
authors.forename: Ming-Wei
authors.initials: MW
authors.lastname: Wang
authors.forename: En-Zhi
authors.initials: EZ
authors.lastname: Jia
authors.forename: Zhi-Jian
authors.initials: ZJ
authors.lastname: Yang
authors.forename: Jun
authors.initials: J
authors.lastname: Huang
mesh_terms: D054392:Adipokines / Q000378:metabolism; D000368:Aged; D002097:C-Reactive Protein / Q000235:genetics; D003324:Coronary Artery Disease / Q000235:genetics*; D005260:Female; D005838:Genotype; D006801:Humans; D007249:Inflammation / Q000235:genetics*; D015850:Interleukin-6 / Q000235:genetics; D008297:Male; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood* / Q000235:genetics*; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic; D012737:Sex Factors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D054392:Adipokines; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D054409:Nicotinamide Phosphoribosyltransferase
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