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      Tumor necrosis factor-alpha G-238A polymorphism and coronary artery disease risk: a meta-analysis of 4,222 patients and 4,832 controls

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          The aim of the present study was to investigate the association between tumor necrosis factor-alpha (TNF-α) gene G-238A polymorphism and risk of coronary artery disease (CAD) using a meta-analytical approach.


          The PubMed and Embase databases were searched for relevant publications up to January 13, 2015. Four authors (XPH, XDZ, XTZ, and ZJZ) independently selected the studies, extracted, and analyzed the data using the Comprehensive Meta-Analysis software. The sensitivity and subgroups analyses were also performed. Either a fixed effects or a random effects model was used to estimate pooled odds ratios (ORs) and their 95% confidence intervals (CIs).


          Finally, ten articles including eleven case-control studies involving 4,222 patients and 4,832 controls were yielded. The results indicated no significant association between G-238A polymorphism and CAD risk (A vs G: OR =1.08, 95% CI =0.89–1.30; AA vs GG: OR =1.15, 95% CI =0.59–2.25; GA vs GG: OR =1.14, 95% CI =0.88–1.48; AA vs [GG + GA]: OR =1.09, 95% CI =0.56–2.14; (GA + AA) vs GG: OR =1.11, 95% CI =0.90–1.38). In the subgroup analyses, similar results were obtained with overall populations. The sensitivity analyses showed that the overall results were robust. No publication bias was detected.


          Based on current evidence, we can conclude that TNF-α G-238A polymorphism might not be associated with CAD risk.

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          Most cited references 45

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          Cardiovascular disease epidemiology in Asia: an overview.

          Cardiovascular disease (CVD) is the leading cause of death in the world and half of the cases of CVD are estimated to occur in Asia. Compared with Western countries, most Asian countries, except for Japan, South Korea, Singapore and Thailand, have higher age-adjusted mortality from CVD. In Japan, the mortality from CVD, especially stroke, has declined continuously from the 1960s to the 2000s, which has contributed to making Japan into the top-ranking country for longevity in the world. Hypertension and smoking are the most notable risk factors for stroke and coronary artery disease, whereas dyslipidemia and diabetes mellitus are risk factors for ischemic heart disease and ischemic stroke. The nationwide approach to hypertension prevention and control has contributed to a substantial decline in stroke mortality in Japan. Recent antismoking campaigns have contributed to a decline in the smoking rate among men. Conversely, the prevalence of dyslipidemia and diabetes mellitus increased from the 1980s to the 2000s and, therefore, the population-attributable risks of CVD for dyslipidemia and diabetes mellitus have increased moderately. To prevent future CVD in Asia, the intensive prevention programs for hypertension and smoking should be continued and that for emerging metabolic risk factors should be intensified in Japan. The successful intervention programs in Japan can be applied to other Asian countries.
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              Age-related loss of CpG methylation in the tumour necrosis factor promoter.

              Dysregulated production of TNF has been implicated in the pathogenesis and severity of inflammatory rheumatic diseases, many of which show age-related increased incidence. Ageing is also associated with changes in the immune system including higher systemic levels of pro-inflammatory cytokines. Methylation of DNA is an important regulator of gene expression and changes with age. In this study we investigated whether the DNA methylation status of the TNF promoter changed with age in peripheral blood leucocytes and macrophages. Using pyrosequencing assays we detected age-related demethylation of CpG motifs (-304, -245 and -239) in the TNF promoter in human peripheral blood cells from 312 healthy controls (0.8% per decade, confidence interval (CI)=0.44-1.13%, p=1×10(-5)) and primary monocyte-derived macrophages (MDM) from a separate population of 78 healthy controls (1.4% per decade, CI=0.79-2.13%, p=7×10(-5)). Methylation a TNF promoter fragment (-345-+154) resulted in 78% reduction of reporter gene activity compared with the unmethylated promoter construct. These data suggest a potential role of accrued changes in DNA methylation in the development of age-related inflammatory diseases, such as rheumatoid arthritis and polymyalgia rheumatica, in which TNF is a pivotal mediator. Copyright © 2011 Elsevier Ltd. All rights reserved.

                Author and article information

                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                23 September 2015
                : 11
                : 1429-1436
                [1 ]Department of Cardiology, Suizhou Hospital, Hubei University of Medicine, Suizhou, Hubei Province, People’s Republic of China
                [2 ]Department of Cardiology and 4th Cadres Ward, General Hospital of Beijing Military Command, Beijing, People’s Republic of China
                [3 ]Chinese Evidence-Based Medicine Center and Chinese Cochrane Center, West China Hospital, Sichuan University, Chengdu, People’s Republic of China
                [4 ]Center for Evidence-Based and Translational Medicine, Zhongnan Hospital, Wuhan University, Wuhan, People’s Republic of China
                Author notes
                Correspondence: Wan-Lin Wei, Department of Cardiology and 4th Cadres Ward, General Hospital of Beijing Military Command, No 5 Nan Men Cang, Dongcheng, Beijing 100125, People’s Republic of China, Tel +86 10 8400 8479, Email weiwanlin2012@ 123456126.com

                These authors contributed equally to this work

                © 2015 Hua et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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