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Original Research

Aldehyde dehydrogenase 2 rs671G>A polymorphism and ischemic stroke risk in Chinese population: a meta-analysis

, , , , &
Pages 1015-1029 | Published online: 23 Apr 2019
 

Abstract

Introduction: Recently, molecular epidemiological studies have suggested that aldehyde dehydrogenase 2 (ALDH2) rs671 G>A polymorphism may be a risk factor for ischemic stroke (IS). However, the results reported have not been consistent.

Methods: We conducted the meta-analysis to explore the precise association between ALDH2 rs671 G>A polymorphism and IS risk. Five online databases were searched and the relative studies were reviewed from inception to October 1, 2018. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated in each genetic model of the general and subgroup. Furthermore, the heterogeneity, accumulative analyses, sensitivity analyses and publication bias were calculated simultaneously.

Results: Overall, nine case-control studies involving 6,129 subjects were included in this meta-analysis. All studies were focused on the Chinese population and some significant associations were found between ALDH2 rs671 G>A polymorphism and IS risk (A vs G: OR=1.29, 95% CI=1.01–1.65, P=0.04, I2=78.2%; AA vs GG: OR=1.86, 95% CI=1.27–2.21, P<0.01, I2=11.3%; AA vs GG + GA: OR=1.67, 95% CI=1.27–2.19, P<0.01, I2=0%). Some significant and similar results were also observed in the subgroup analysis.

Conclusion: Our meta-analysis indicates that the ALDH2 rs671 G>A polymorphism may play an important role in the occurrence of IS by reducing the activity of ALDH2 and interfering with the metabolic processes involving acetaldehyde.

Acknowledgments

This study was supported by the Foundations of the Science and Technology Department of Hubei Province (No. 2016CFB567), and the Hubei Province health and family planning scientific research project (No. WJ2017F069). The funders had no roles in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Disclosure

The authors report no conflcits of interest in this work.

Supplementary materials

Figure S1 OR and 95% CIs of the associations between ALDH2 rs671G>A polymorphism and ischemic stroke risk (A for A vs G model; B for GA vs GG model; C for GA + AA vs GG model; D for AA vs GG + GA model).

Figure S1 OR and 95% CIs of the associations between ALDH2 rs671G>A polymorphism and ischemic stroke risk (A for A vs G model; B for GA vs GG model; C for GA + AA vs GG model; D for AA vs GG + GA model).

Figure S2 Cumulative meta-analyses according to publication year in ALDH2 rs671G>A polymorphism and ischemic stroke risk (A for A vs G model; B for GA vs GG model; C for GA + AA vs GG model; D for AA vs GG + GA model).

Figure S2 Cumulative meta-analyses according to publication year in ALDH2 rs671G>A polymorphism and ischemic stroke risk (A for A vs G model; B for GA vs GG model; C for GA + AA vs GG model; D for AA vs GG + GA model).

Figure S3 Sensitivity analysis through deleting each study to reflect the influence of the individual dataset to the pooled ORs in ALDH2 rs671G>A polymorphism and ischemic stroke risk (A for A vs G model; B for GA vs GG model; C for GA + AA vs GG model; D for AA vs GG + GA model).

Figure S3 Sensitivity analysis through deleting each study to reflect the influence of the individual dataset to the pooled ORs in ALDH2 rs671G>A polymorphism and ischemic stroke risk (A for A vs G model; B for GA vs GG model; C for GA + AA vs GG model; D for AA vs GG + GA model).

Figure S4 Funnel plot analysis to detect publication bias in ALDH2 rs671G>A polymorphism (A for A vs G model; B for GA vs GG model; C for GA + AA vs GG model; D for AA vs GG + GA model). Circles represent the weight of the studies.

Figure S4 Funnel plot analysis to detect publication bias in ALDH2 rs671G>A polymorphism (A for A vs G model; B for GA vs GG model; C for GA + AA vs GG model; D for AA vs GG + GA model). Circles represent the weight of the studies.