Genetic Variants Associated with Chronic Obstructive Pulmonary Disease Risk: Cumulative Epidemiological Evidence from Meta-Analyses and Genome-Wide Association Studies

Background. Last two decades, many association studies on genetic variants and chronic obstructive pulmonary disease (COPD) risk have been published. But results from different studies are inconsistent. Therefore, we performed this article to systematically evaluate results from previous meta-analys...

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Main Authors: Caiyang Liu, Ran Ran, Xiaoliang Li, Gaohua Liu, Xiaoyang Xie, Ji Li
Format: Article
Language:English
Published: Wiley 2022-01-01
Series:Canadian Respiratory Journal
Online Access:http://dx.doi.org/10.1155/2022/3982335
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author Caiyang Liu
Ran Ran
Xiaoliang Li
Gaohua Liu
Xiaoyang Xie
Ji Li
author_facet Caiyang Liu
Ran Ran
Xiaoliang Li
Gaohua Liu
Xiaoyang Xie
Ji Li
author_sort Caiyang Liu
collection DOAJ
description Background. Last two decades, many association studies on genetic variants and chronic obstructive pulmonary disease (COPD) risk have been published. But results from different studies are inconsistent. Therefore, we performed this article to systematically evaluate results from previous meta-analyses and genome-wide association studies (GWASs). Material and Methods. Firstly, we retrieved meta-analyses in PubMed, Embase, and China National Knowledge Infrastructure and GWASs in PubMed and GWAS catalog on or before April 7th, 2022. Then, data were extracted and screened. Finally, two main methods—Venice criteria and false-positive report probability test—were used to evaluate significant associations. Results. As a result, eighty-eight meta-analyses and 5 GWASs were deemed eligible for inclusion. Fifty variants in 26 genes obtained from meta-analyses were significantly associated with COPD risk. Cumulative epidemiological evidence of an association was graded as strong for 10 variants in 8 genes (GSTM1, CHRNA, ADAM33, SP-D, TNF-α, VDBP, HMOX1, and HHIP), moderate for 6 variants in 5 genes (PI, GSTM1, ADAM33, TNF-α, and VDBP), and weak for 40 variants in 23 genes. Five variants in 4 genes showed convincing evidence of no association with COPD risk in meta-analyses. Additionally, 29 SNPs identified in GWASs were proved to be noteworthy based on the FPRP test. Conclusion. In summary, more than half (52.38%) of genetic variants reported in previous meta-analyses showed no association with COPD risk. However, 13 variants in 9 genes had moderate to strong evidence for an association. This article can serve as a useful reference for further studies.
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spelling doaj-art-6c8d47e9092f4f8cb5dc80f7df9250be2025-02-03T01:07:22ZengWileyCanadian Respiratory Journal1916-72452022-01-01202210.1155/2022/3982335Genetic Variants Associated with Chronic Obstructive Pulmonary Disease Risk: Cumulative Epidemiological Evidence from Meta-Analyses and Genome-Wide Association StudiesCaiyang Liu0Ran Ran1Xiaoliang Li2Gaohua Liu3Xiaoyang Xie4Ji Li5Department of Cardiothoracic SurgeryBreast Surgery Center of Sichuan Cancer HospitalDepartment of Cardiothoracic SurgeryDepartment of Cardiothoracic SurgeryDepartment of Cardiothoracic SurgeryDepartment of Cardiothoracic SurgeryBackground. Last two decades, many association studies on genetic variants and chronic obstructive pulmonary disease (COPD) risk have been published. But results from different studies are inconsistent. Therefore, we performed this article to systematically evaluate results from previous meta-analyses and genome-wide association studies (GWASs). Material and Methods. Firstly, we retrieved meta-analyses in PubMed, Embase, and China National Knowledge Infrastructure and GWASs in PubMed and GWAS catalog on or before April 7th, 2022. Then, data were extracted and screened. Finally, two main methods—Venice criteria and false-positive report probability test—were used to evaluate significant associations. Results. As a result, eighty-eight meta-analyses and 5 GWASs were deemed eligible for inclusion. Fifty variants in 26 genes obtained from meta-analyses were significantly associated with COPD risk. Cumulative epidemiological evidence of an association was graded as strong for 10 variants in 8 genes (GSTM1, CHRNA, ADAM33, SP-D, TNF-α, VDBP, HMOX1, and HHIP), moderate for 6 variants in 5 genes (PI, GSTM1, ADAM33, TNF-α, and VDBP), and weak for 40 variants in 23 genes. Five variants in 4 genes showed convincing evidence of no association with COPD risk in meta-analyses. Additionally, 29 SNPs identified in GWASs were proved to be noteworthy based on the FPRP test. Conclusion. In summary, more than half (52.38%) of genetic variants reported in previous meta-analyses showed no association with COPD risk. However, 13 variants in 9 genes had moderate to strong evidence for an association. This article can serve as a useful reference for further studies.http://dx.doi.org/10.1155/2022/3982335
spellingShingle Caiyang Liu
Ran Ran
Xiaoliang Li
Gaohua Liu
Xiaoyang Xie
Ji Li
Genetic Variants Associated with Chronic Obstructive Pulmonary Disease Risk: Cumulative Epidemiological Evidence from Meta-Analyses and Genome-Wide Association Studies
Canadian Respiratory Journal
title Genetic Variants Associated with Chronic Obstructive Pulmonary Disease Risk: Cumulative Epidemiological Evidence from Meta-Analyses and Genome-Wide Association Studies
title_full Genetic Variants Associated with Chronic Obstructive Pulmonary Disease Risk: Cumulative Epidemiological Evidence from Meta-Analyses and Genome-Wide Association Studies
title_fullStr Genetic Variants Associated with Chronic Obstructive Pulmonary Disease Risk: Cumulative Epidemiological Evidence from Meta-Analyses and Genome-Wide Association Studies
title_full_unstemmed Genetic Variants Associated with Chronic Obstructive Pulmonary Disease Risk: Cumulative Epidemiological Evidence from Meta-Analyses and Genome-Wide Association Studies
title_short Genetic Variants Associated with Chronic Obstructive Pulmonary Disease Risk: Cumulative Epidemiological Evidence from Meta-Analyses and Genome-Wide Association Studies
title_sort genetic variants associated with chronic obstructive pulmonary disease risk cumulative epidemiological evidence from meta analyses and genome wide association studies
url http://dx.doi.org/10.1155/2022/3982335
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