作者: Jing-Zhang Wang , Wen-Tao Du , Jing Bai , Shu-Zhen Cheng , Yu-Hua Zhang
DOI: 10.1016/J.JSTROKECEREBROVASDIS.2020.104935
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摘要: Abstract Backgrounds Vascular atherosclerosis leads to various cardiovascular and cerebrovascular diseases. Nitric oxide (NO) promotes vasodilatation prevents Coronary Artery Disease (CAD). Pin1 suppresses NO production by down-regulating the activity of endothelial nitric synthase (eNOS). Whether genetic polymorphisms PIN1 gene (encoding Pin1) are implicated in CAD deserves investigations human beings. Methods A total 210 patients control individuals (all females) were enrolled, their genotypes rs2233679 (–667C/T, a key SNP promoter gene) sequenced. T-test, chi-square test, odds ratio (OR) 95% confidence interval (95% CI) calculated evaluate Hardy–Weinberg equilibrium, varied distribution relative risk. Results The differences age, BMI, triglyceride, cholesterol, low-density high density cholesterol between groups not significant P>0.05), Hardy-Weinberg equilibrium was observed two (both P>0.05). frequency –667T allele group higher than that group. genotype –667TT elicited hazardous risk compared –667CC (OR=1.85, CI: 0.75-4.53) as well CC+CT (OR=1.97, 0.86-4.49). Conclusions We firstly show may elicit CAD-risk –667C, be new biomarker for increased incidence CAD. These novel observations put forward understanding PIN1-CAD relationship humans, potentially contributing both disorders.