Glutathione S-Transferase T1 (GSTT1) Null Polymorphism, Smoking, and Their Interaction in Coronary Heart Disease: A Comprehensive Meta-Analysis

被引:22
作者
Song, Yadong [1 ,3 ]
Shan, Zhilei [2 ,3 ]
Luo, Cheng [2 ,3 ]
Kang, Cuixin [1 ]
Yang, Yong [1 ]
He, Ping [1 ]
Li, Shoudao [1 ]
Chen, Liangkai [2 ,3 ]
Jiang, Xiaoming [1 ]
Liu, Liegang [2 ,3 ]
机构
[1] Wuhan Inst Food & Cosmet Control, Wuhan 430012, Peoples R China
[2] Tongji Med Coll, Sch Publ Hlth, Key Lab Environm & Hlth, Minist Educ, Wuhan, Peoples R China
[3] Huazhong Univ Sci & Technol, Tongji Med Coll, Hubei Key Lab Food Nutr & Safety, Dept Nutr & Food Hyg, Wuhan 430030, Peoples R China
关键词
Meta-analysis; Coronary heart disease; GSTT1; Smoking; Genetic polymorphism; CASE-ONLY DESIGNS; ARTERY-DISEASE; SUSCEPTIBILITY FACTOR; MYOCARDIAL-INFARCTION; MOLECULAR-MECHANISMS; LIPID-PEROXIDATION; GENE POLYMORPHISMS; RISK-FACTOR; ASSOCIATION; ATHEROSCLEROSIS;
D O I
10.1016/j.hlc.2016.07.005
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background The association between glutathione S-transferase T1 (GSTT1) null polymorphism and coronary heart disease (CHD) is inconsistent among studies, and data on the GSTT1 null genotype-smoking interplay in CHD is lacking. We conducted this meta-analysis to investigate the relationship between GSTT1 null polymorphism and CHD and to assess the potential interaction between GSTT1 null genotype and smoking. Methods PubMed and EMBASE databases were searched up to 27 January 2016 using the appropriate terms. Odds ratios were pooled using either fixed-effects or random-effects models. Results Twenty-nine articles including 31 studies with 15,004 cases and 35,597 controls were eligible. The randomeffects model showed that the GSTT1 null genotype was associated with increased CHD risk (OR = 1.213, 95% CI: 1.004-1.467; I-2 = 90.4%). After excluding 10 studies detected by Galbraith plot, the fixed effects summary estimate also showed an increased risk of CHD (OR = 1.14, 95% CI: 1.06-1.22; I-2 = 27.7%). A case-only analysis including eight studies showed a statistically significant positive interaction between GSTT1 null polymorphism and smoking status on CHD (OR = 1.34, 95% CI: 1.09-1.64; I-2 = 0%). Sensitivity analyses further supported the associations. No publication bias was observed. Conclusions This meta-analysis suggests that GSTT1 null polymorphism is associated with the risk of CHD. To our knowledge, this is the first meta-analysis to prove a positive effect of the interaction between GSTT1 null genotype and smoking status on the risk of CHD. Future studies with detailed individual information are needed to confirm our findings.
引用
收藏
页码:362 / 370
页数:9
相关论文
共 57 条
[1]   Tnull and Mnull genotypes of the glutathione S-transferase gene are risk factor for CAD independent of smoking [J].
Abu-Amero, KK ;
Al-Boudari, OM ;
Mohamed, GH ;
Dzimiri, N .
BMC MEDICAL GENETICS, 2006, 7
[2]  
Andreassi MG, 2000, ENVIRON MOL MUTAGEN, V35, P265, DOI 10.1002/1098-2280(2000)35:4<265::AID-EM1>3.0.CO
[3]  
2-M
[4]   DNA damage as a new emerging risk factor in Atherosclerosis [J].
Andreassi, MG ;
Botto, N .
TRENDS IN CARDIOVASCULAR MEDICINE, 2003, 13 (07) :270-275
[5]  
[Anonymous], 2010, HUM GENOMICS PROTEOM, DOI DOI 10.4061/2010/876940
[6]  
Bazo Ana Paula, 2011, Cardiovasc Pathol, V20, pe9, DOI 10.1016/j.carpath.2009.12.004
[7]   Marine glutathione S-transferases [J].
Blanchette, Brian ;
Feng, Xia ;
Singh, Bal Ram .
MARINE BIOTECHNOLOGY, 2007, 9 (05) :513-542
[8]   Glutathione S-transferase M1 and T1 genotypes and myocardial infarction [J].
Cora, Tulin ;
Tokac, Mehmet ;
Acar, Hasan ;
Soylu, Ahmet ;
Inan, Ziya .
MOLECULAR BIOLOGY REPORTS, 2013, 40 (04) :3263-3267
[9]   GSTT1 genotype modifies the association between cruciferous vegetable intake and the risk of myocardial infarction [J].
Cornelis, Marilyn C. ;
El-Sohemy, Ahmed ;
Campos, Hannia .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 2007, 86 (03) :752-758
[10]   Mutagenesis and cardiovascular diseases Molecular mechanisms, risk factors, and protective factors [J].
De Flora, Silvio ;
Izzotti, Alberto .
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 2007, 621 (1-2) :5-17