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Association between polymorphisms in interleukin-18 promoter and risk of coronary artery disease: a meta-analysis

Background: Previous studies have explored associations between interleukin-18 (IL-18) promoter polymorphisms and coronary artery disease (CAD). However, the results were controversial. We conducted a meta-analysis to clarify the association between the two polymorphisms and CAD risk. Methods: We se...

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Autores principales: Lian, Zheng, Li, Su-Fang, Cui, Yu-Xia, Wu, Man-Yan, Su, Li-Na, Hu, Dan, Xiong, Wei-Jue, Chen, Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6863765/
https://www.ncbi.nlm.nih.gov/pubmed/31661113
http://dx.doi.org/10.1042/BSR20192721
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author Lian, Zheng
Li, Su-Fang
Cui, Yu-Xia
Wu, Man-Yan
Su, Li-Na
Hu, Dan
Xiong, Wei-Jue
Chen, Hong
author_facet Lian, Zheng
Li, Su-Fang
Cui, Yu-Xia
Wu, Man-Yan
Su, Li-Na
Hu, Dan
Xiong, Wei-Jue
Chen, Hong
author_sort Lian, Zheng
collection PubMed
description Background: Previous studies have explored associations between interleukin-18 (IL-18) promoter polymorphisms and coronary artery disease (CAD). However, the results were controversial. We conducted a meta-analysis to clarify the association between the two polymorphisms and CAD risk. Methods: We searched English and Chinese databases and calculated the odds ratio (OR) and 95% confidence interval (CI) to estimate whether there are genetic associations between IL-18 promoter polymorphisms and the risk of CAD. All relevant studies were screened and meta-analyzed using STATA 15.0. Results: A total of 15 studies, including 12 studies for -137 G/C and 9 studies for -607 C/A, were identified for the meta-analysis. For -137 G/C, the results showed a significantly reduced risk of CAD in the dominant model (OR = 0.85) and heterozygous model (OR = 0.88) in the overall analysis. However, in subgroup analysis, decreased CAD risks were only observed in Asian populations for heterozygous genetic models. For -607 C/A, the overall OR revealed a reduced risk of CAD in all five genetic models (allelic, OR = 0.78; recessive, OR = 0.75; dominant, OR = 0.68; homozygous, OR = 0.61; heterozygous, OR = 0.72). In subgroup analysis, reduced CAD risk was also found in five genetic models of the Asian population. We also found that the IL-18 polymorphisms were correlated with myocardial infarction (MI) and multivessel (MV) disease. Conclusion: Our results suggested that the -137 polymorphism and -607 polymorphism in the IL-18 promoter were negatively associated with CAD, especially in the Asian population. In addition, some genetic models were correlated with the severity of CAD.
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spelling pubmed-68637652019-12-03 Association between polymorphisms in interleukin-18 promoter and risk of coronary artery disease: a meta-analysis Lian, Zheng Li, Su-Fang Cui, Yu-Xia Wu, Man-Yan Su, Li-Na Hu, Dan Xiong, Wei-Jue Chen, Hong Biosci Rep Cardiovascular System & Vascular Biology Background: Previous studies have explored associations between interleukin-18 (IL-18) promoter polymorphisms and coronary artery disease (CAD). However, the results were controversial. We conducted a meta-analysis to clarify the association between the two polymorphisms and CAD risk. Methods: We searched English and Chinese databases and calculated the odds ratio (OR) and 95% confidence interval (CI) to estimate whether there are genetic associations between IL-18 promoter polymorphisms and the risk of CAD. All relevant studies were screened and meta-analyzed using STATA 15.0. Results: A total of 15 studies, including 12 studies for -137 G/C and 9 studies for -607 C/A, were identified for the meta-analysis. For -137 G/C, the results showed a significantly reduced risk of CAD in the dominant model (OR = 0.85) and heterozygous model (OR = 0.88) in the overall analysis. However, in subgroup analysis, decreased CAD risks were only observed in Asian populations for heterozygous genetic models. For -607 C/A, the overall OR revealed a reduced risk of CAD in all five genetic models (allelic, OR = 0.78; recessive, OR = 0.75; dominant, OR = 0.68; homozygous, OR = 0.61; heterozygous, OR = 0.72). In subgroup analysis, reduced CAD risk was also found in five genetic models of the Asian population. We also found that the IL-18 polymorphisms were correlated with myocardial infarction (MI) and multivessel (MV) disease. Conclusion: Our results suggested that the -137 polymorphism and -607 polymorphism in the IL-18 promoter were negatively associated with CAD, especially in the Asian population. In addition, some genetic models were correlated with the severity of CAD. Portland Press Ltd. 2019-11-19 /pmc/articles/PMC6863765/ /pubmed/31661113 http://dx.doi.org/10.1042/BSR20192721 Text en © 2019 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).
spellingShingle Cardiovascular System & Vascular Biology
Lian, Zheng
Li, Su-Fang
Cui, Yu-Xia
Wu, Man-Yan
Su, Li-Na
Hu, Dan
Xiong, Wei-Jue
Chen, Hong
Association between polymorphisms in interleukin-18 promoter and risk of coronary artery disease: a meta-analysis
title Association between polymorphisms in interleukin-18 promoter and risk of coronary artery disease: a meta-analysis
title_full Association between polymorphisms in interleukin-18 promoter and risk of coronary artery disease: a meta-analysis
title_fullStr Association between polymorphisms in interleukin-18 promoter and risk of coronary artery disease: a meta-analysis
title_full_unstemmed Association between polymorphisms in interleukin-18 promoter and risk of coronary artery disease: a meta-analysis
title_short Association between polymorphisms in interleukin-18 promoter and risk of coronary artery disease: a meta-analysis
title_sort association between polymorphisms in interleukin-18 promoter and risk of coronary artery disease: a meta-analysis
topic Cardiovascular System & Vascular Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6863765/
https://www.ncbi.nlm.nih.gov/pubmed/31661113
http://dx.doi.org/10.1042/BSR20192721
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