{"title":"Contribution of Glutathione-S-Transferases Polymorphism and Risk of Coronary Artery Diseases: A Meta-Analysis.","authors":"S. S, K. K","doi":"10.2174/1874609815666220304193925","DOIUrl":null,"url":null,"abstract":"BACKGROUND\nOxidative stress is one of the risk components in the development of coronary artery diseases (CAD) and polymorphism in major antioxidant genes like Glutathione-S-Transferases (GST) has been associated with the increased CAD susceptibility and severity.\n\n\nOBJECTIVE\nTo get a precise evaluation and to update the association, a meta-analysis on GST (GSTM1, GSTT1 and GSTP1) polymorphism with CAD was performed. Moreover, the combined effect of GSTM1/GSTT1 null genotypes on CAD risk which is not yet studied so far but it has the highest risk of developing diseases.\n\n\nMATERIALS AND METHOD\nPubMed, Embase and Web of Science were systematically searched for eligible studies. Case-control studies with genotypic frequency, provide data to calculate odds ratio (OR) and in English language were selected. OR with 95% C.I was calculated and random effect model was used. NOS scale was used to asses the qulity of the included studies.\n\n\nRESULTS\nMeta-analysis indicated that the GSTM1 null genotype and GSTP1 (Ile105Val) polymorphism is significantly associated with CAD risk with a pooled OR-1.38, p=0.01 for GSTM1 and OR-1.19, p=0.04 for GSTP1. Dual null genotype of GSTM1-GSTT1 has highest risk for CAD development (OR-1.59, p=0.003) and there is no significant association for GSTT1 null genotype with CAD. In the subgroup analysis, GSTM1 showed the increased risk for Asians (OR-1.68, p=<0.01) and smokers (OR-1.98, p=<0.01). Publication bias was not observed.\n\n\nCONCLUSION\nThe findings suggests that the GSTM1/GSTP1 polymorphism can be a predictive factor for CAD risk and a larger sample size is required further to confirm the association.","PeriodicalId":11008,"journal":{"name":"Current aging science","volume":"71 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current aging science","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1874609815666220304193925","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 2
Abstract
BACKGROUND
Oxidative stress is one of the risk components in the development of coronary artery diseases (CAD) and polymorphism in major antioxidant genes like Glutathione-S-Transferases (GST) has been associated with the increased CAD susceptibility and severity.
OBJECTIVE
To get a precise evaluation and to update the association, a meta-analysis on GST (GSTM1, GSTT1 and GSTP1) polymorphism with CAD was performed. Moreover, the combined effect of GSTM1/GSTT1 null genotypes on CAD risk which is not yet studied so far but it has the highest risk of developing diseases.
MATERIALS AND METHOD
PubMed, Embase and Web of Science were systematically searched for eligible studies. Case-control studies with genotypic frequency, provide data to calculate odds ratio (OR) and in English language were selected. OR with 95% C.I was calculated and random effect model was used. NOS scale was used to asses the qulity of the included studies.
RESULTS
Meta-analysis indicated that the GSTM1 null genotype and GSTP1 (Ile105Val) polymorphism is significantly associated with CAD risk with a pooled OR-1.38, p=0.01 for GSTM1 and OR-1.19, p=0.04 for GSTP1. Dual null genotype of GSTM1-GSTT1 has highest risk for CAD development (OR-1.59, p=0.003) and there is no significant association for GSTT1 null genotype with CAD. In the subgroup analysis, GSTM1 showed the increased risk for Asians (OR-1.68, p=<0.01) and smokers (OR-1.98, p=<0.01). Publication bias was not observed.
CONCLUSION
The findings suggests that the GSTM1/GSTP1 polymorphism can be a predictive factor for CAD risk and a larger sample size is required further to confirm the association.