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Apolipoprotein A1 polymorphisms and risk of coronary artery disease: a meta-analysis

INTRODUCTION: It has been reported that APOA1 –75G/A polymorphism might be associated with susceptibility to coronary artery disease (CAD). Owing to mixed and inconclusive results, we conducted a meta-analysis to systematically summarize and clarify the association between APOA1-75G/A polymorphism a...

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Autores principales: Xu, Lang-Biao, Zhou, Ya-Feng, Yao, Jia-Lu, Sun, Si-Jia, Rui, Qing, Yang, Xiang-Jun, Li, Xiao-Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5510497/
https://www.ncbi.nlm.nih.gov/pubmed/28721149
http://dx.doi.org/10.5114/aoms.2017.65233
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author Xu, Lang-Biao
Zhou, Ya-Feng
Yao, Jia-Lu
Sun, Si-Jia
Rui, Qing
Yang, Xiang-Jun
Li, Xiao-Bo
author_facet Xu, Lang-Biao
Zhou, Ya-Feng
Yao, Jia-Lu
Sun, Si-Jia
Rui, Qing
Yang, Xiang-Jun
Li, Xiao-Bo
author_sort Xu, Lang-Biao
collection PubMed
description INTRODUCTION: It has been reported that APOA1 –75G/A polymorphism might be associated with susceptibility to coronary artery disease (CAD). Owing to mixed and inconclusive results, we conducted a meta-analysis to systematically summarize and clarify the association between APOA1-75G/A polymorphism and the risk of CAD. MATERIAL AND METHODS: A systematic search of studies on the association of single nucleotide polymorphisms (SNP) with susceptibility to CAD was conducted. A total of 9 case-control studies (1864 cases and 1196 controls) on the APOA1-75G/A polymorphism were included. RESULTS: We observed no statistically significant association between APOA1 –75G/A polymorphism and risk of CAD under the dominant genetic model (AA + AG vs. GG: OR = 1.03, 95% CI: 0.65–1.66), allelic contrast (A vs. G: OR = 0.88, 95% CI: 0.58–1.32), heterozygote model (AG vs. GG: OR = 1.24, 95% CI: 0.81–1.89) or homozygote model (AA vs. GG: OR = 0.52, 95% CI: 0.26–1.05). Significant heterogeneity between individual studies appears in all five models, but a strong association under the recessive genetic model (AA vs. AG + GG: OR = 0.51, 95% CI: 0.28–0.92). In the subgroup analysis by Hardy-Weinberg equilibrium (HWE; the presence or absence of HWE in controls), significantly decreased CAD risk and no significant heterogeneity were observed among controls consistent with HWE. Overall, the APOA1 A allele is one of the protective factors of CAD. A stronger association between APOA1-75G/A polymorphisms and CAD risk was present in the studies consistent with HWE. CONCLUSIONS: The minor allele of the APOA1-75G/A polymorphism is a protective factor for CAD, especially in the studies consistent with HWE.
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spelling pubmed-55104972017-07-18 Apolipoprotein A1 polymorphisms and risk of coronary artery disease: a meta-analysis Xu, Lang-Biao Zhou, Ya-Feng Yao, Jia-Lu Sun, Si-Jia Rui, Qing Yang, Xiang-Jun Li, Xiao-Bo Arch Med Sci Clinical Research INTRODUCTION: It has been reported that APOA1 –75G/A polymorphism might be associated with susceptibility to coronary artery disease (CAD). Owing to mixed and inconclusive results, we conducted a meta-analysis to systematically summarize and clarify the association between APOA1-75G/A polymorphism and the risk of CAD. MATERIAL AND METHODS: A systematic search of studies on the association of single nucleotide polymorphisms (SNP) with susceptibility to CAD was conducted. A total of 9 case-control studies (1864 cases and 1196 controls) on the APOA1-75G/A polymorphism were included. RESULTS: We observed no statistically significant association between APOA1 –75G/A polymorphism and risk of CAD under the dominant genetic model (AA + AG vs. GG: OR = 1.03, 95% CI: 0.65–1.66), allelic contrast (A vs. G: OR = 0.88, 95% CI: 0.58–1.32), heterozygote model (AG vs. GG: OR = 1.24, 95% CI: 0.81–1.89) or homozygote model (AA vs. GG: OR = 0.52, 95% CI: 0.26–1.05). Significant heterogeneity between individual studies appears in all five models, but a strong association under the recessive genetic model (AA vs. AG + GG: OR = 0.51, 95% CI: 0.28–0.92). In the subgroup analysis by Hardy-Weinberg equilibrium (HWE; the presence or absence of HWE in controls), significantly decreased CAD risk and no significant heterogeneity were observed among controls consistent with HWE. Overall, the APOA1 A allele is one of the protective factors of CAD. A stronger association between APOA1-75G/A polymorphisms and CAD risk was present in the studies consistent with HWE. CONCLUSIONS: The minor allele of the APOA1-75G/A polymorphism is a protective factor for CAD, especially in the studies consistent with HWE. Termedia Publishing House 2017-01-19 2017-06 /pmc/articles/PMC5510497/ /pubmed/28721149 http://dx.doi.org/10.5114/aoms.2017.65233 Text en Copyright: © 2017 Termedia & Banach http://creativecommons.org/licenses/by-nc-sa/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
spellingShingle Clinical Research
Xu, Lang-Biao
Zhou, Ya-Feng
Yao, Jia-Lu
Sun, Si-Jia
Rui, Qing
Yang, Xiang-Jun
Li, Xiao-Bo
Apolipoprotein A1 polymorphisms and risk of coronary artery disease: a meta-analysis
title Apolipoprotein A1 polymorphisms and risk of coronary artery disease: a meta-analysis
title_full Apolipoprotein A1 polymorphisms and risk of coronary artery disease: a meta-analysis
title_fullStr Apolipoprotein A1 polymorphisms and risk of coronary artery disease: a meta-analysis
title_full_unstemmed Apolipoprotein A1 polymorphisms and risk of coronary artery disease: a meta-analysis
title_short Apolipoprotein A1 polymorphisms and risk of coronary artery disease: a meta-analysis
title_sort apolipoprotein a1 polymorphisms and risk of coronary artery disease: a meta-analysis
topic Clinical Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5510497/
https://www.ncbi.nlm.nih.gov/pubmed/28721149
http://dx.doi.org/10.5114/aoms.2017.65233
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