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Association of IL‐10‐1082A/G polymorphism with cardiovascular disease risk: Evidence from a case–control study to an updated meta‐analysis
BACKGROUND: Previous studies have generated controversial results about the association of interleukin 10 (IL‐10) gene polymorphisms (−1082G/A) in the progression of cardiovascular disease (CVD). Therefore, this study processed a systemic meta‐analysis to verify this association. METHODS: The public...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6825845/ https://www.ncbi.nlm.nih.gov/pubmed/31571432 http://dx.doi.org/10.1002/mgg3.888 |
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author | Lu, Shijuan Zhong, Jianghua Huang, Kang Zhou, Honghao |
author_facet | Lu, Shijuan Zhong, Jianghua Huang, Kang Zhou, Honghao |
author_sort | Lu, Shijuan |
collection | PubMed |
description | BACKGROUND: Previous studies have generated controversial results about the association of interleukin 10 (IL‐10) gene polymorphisms (−1082G/A) in the progression of cardiovascular disease (CVD). Therefore, this study processed a systemic meta‐analysis to verify this association. METHODS: The publication studies on the IL‐10 (−1082G/A) polymorphism and CVDs risk were obtained by searching PubMed and Embase databases. We analyzed the genotype data for meta‐analysis. The results were evaluated by odds ratios (ORs) and 95% confidence intervals (CIs). Meanwhile, our meta‐analysis was also performed sensitivity analyses, heterogeneity test, and identification of publication bias. RESULTS: The present meta‐analysis suggested that the risk with allele G is lower than with allele A for CVD. The G allele of IL‐10 (−1082) could increase the risk of CVDs in the 31 case–control studies for all genetic models. (OR = 1.10, 95% CI: 1.04–1.15 for the allele model A vs. G; OR = 0.87, 95% CI: 0.72–1.04 for the dominant model GG+AG vs. AA; OR = 1.03, 95% CI: 1.02–1.05 for the recessive model GG vs. AG + AA; OR = 1.06, 95% CI = 1.03–1.10 for the homozygote comparison model GG vs. AA; and OR = 0.88, 95% CI = 0.73–1.06 for the heterozygote comparison model AG vs. AA). CONCLUSIONS: In genetic models, the association between the IL‐10 (−1082G/A) polymorphism and CVDs risk was significant. This meta‐analysis proposes that the IL‐10 (−1082G/A) polymorphism may serve as a risk factor for CVDs. |
format | Online Article Text |
id | pubmed-6825845 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-68258452019-11-07 Association of IL‐10‐1082A/G polymorphism with cardiovascular disease risk: Evidence from a case–control study to an updated meta‐analysis Lu, Shijuan Zhong, Jianghua Huang, Kang Zhou, Honghao Mol Genet Genomic Med Original Articles BACKGROUND: Previous studies have generated controversial results about the association of interleukin 10 (IL‐10) gene polymorphisms (−1082G/A) in the progression of cardiovascular disease (CVD). Therefore, this study processed a systemic meta‐analysis to verify this association. METHODS: The publication studies on the IL‐10 (−1082G/A) polymorphism and CVDs risk were obtained by searching PubMed and Embase databases. We analyzed the genotype data for meta‐analysis. The results were evaluated by odds ratios (ORs) and 95% confidence intervals (CIs). Meanwhile, our meta‐analysis was also performed sensitivity analyses, heterogeneity test, and identification of publication bias. RESULTS: The present meta‐analysis suggested that the risk with allele G is lower than with allele A for CVD. The G allele of IL‐10 (−1082) could increase the risk of CVDs in the 31 case–control studies for all genetic models. (OR = 1.10, 95% CI: 1.04–1.15 for the allele model A vs. G; OR = 0.87, 95% CI: 0.72–1.04 for the dominant model GG+AG vs. AA; OR = 1.03, 95% CI: 1.02–1.05 for the recessive model GG vs. AG + AA; OR = 1.06, 95% CI = 1.03–1.10 for the homozygote comparison model GG vs. AA; and OR = 0.88, 95% CI = 0.73–1.06 for the heterozygote comparison model AG vs. AA). CONCLUSIONS: In genetic models, the association between the IL‐10 (−1082G/A) polymorphism and CVDs risk was significant. This meta‐analysis proposes that the IL‐10 (−1082G/A) polymorphism may serve as a risk factor for CVDs. John Wiley and Sons Inc. 2019-09-30 /pmc/articles/PMC6825845/ /pubmed/31571432 http://dx.doi.org/10.1002/mgg3.888 Text en © 2019 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Lu, Shijuan Zhong, Jianghua Huang, Kang Zhou, Honghao Association of IL‐10‐1082A/G polymorphism with cardiovascular disease risk: Evidence from a case–control study to an updated meta‐analysis |
title | Association of IL‐10‐1082A/G polymorphism with cardiovascular disease risk: Evidence from a case–control study to an updated meta‐analysis |
title_full | Association of IL‐10‐1082A/G polymorphism with cardiovascular disease risk: Evidence from a case–control study to an updated meta‐analysis |
title_fullStr | Association of IL‐10‐1082A/G polymorphism with cardiovascular disease risk: Evidence from a case–control study to an updated meta‐analysis |
title_full_unstemmed | Association of IL‐10‐1082A/G polymorphism with cardiovascular disease risk: Evidence from a case–control study to an updated meta‐analysis |
title_short | Association of IL‐10‐1082A/G polymorphism with cardiovascular disease risk: Evidence from a case–control study to an updated meta‐analysis |
title_sort | association of il‐10‐1082a/g polymorphism with cardiovascular disease risk: evidence from a case–control study to an updated meta‐analysis |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6825845/ https://www.ncbi.nlm.nih.gov/pubmed/31571432 http://dx.doi.org/10.1002/mgg3.888 |
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