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Critical Reviews™ in Eukaryotic Gene Expression
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ISSN Imprimir: 1045-4403
ISSN En Línea: 2162-6502

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Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukaryotGeneExpr.2017018680
pages 37-46

Association between Methionine Synthase Reductase A66G Polymorphism and Male Infertility: A Meta-Analysis

Weihai Xu
Department of Reproductive and Genetics, Women's Hospital, Zhejiang University, Hangzhou, Zhejiang, 310006, China
Lin Zhang
Reproductive Endocrinology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang, 310014, China
Xiangli Wu
Reproductive Endocrinology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang, 310014, China
Fan Jin
Department of Reproductive and Genetics, Women's Hospital, Zhejiang University, Hangzhou, Zhejiang, 310006, China

SINOPSIS

The aim of this meta-analysis was to assess the methionine synthase reductase (MTRR) gene 66A>G polymorphism and male infertility susceptibility. Studies were identified in PubMed and Embase databases. An odds ratio (OR) was used to assess the relationship between MTRR 66A>G polymorphism and male infertility risk. A total of seven case-control studies containing 1438 patients and 1363 controls were enrolled in the meta-analysis. Our results showed that no association exists between the MTRR 66A>G polymorphism and male infertility risk in the total population (GG vs. AA: OR = 1.29, 95% confidence interval [CI] = 1.00-1.66; GA vs. AA: OR = 1.09, 95% CI = 0.92-1.30; dominant model: OR = 1.13, 95% CI = 0.96-1.34; recessive model: OR = 0.83, 95% CI = 0.67–1.03). In a subgroup analysis by nationality, the 66A>G polymorphism was not associated with male infertility in both Asians and Caucasians. In a subgroup analysis stratified by male infertility type, significant association was found with oligoasthenozoospermia (OAT) (GG vs. AA: OR = 1.83, 95% CI = 1.24-269; GA vs. AA: OR = 1.36, 95% CI = 0.88-2.11; dominant model: OR = 1.51, 95% CI = 1.13-2.01; recessive model: OR = 0.62, 95% CI = 0.46-0.85). In summary, the present meta-analysis suggests that MTRR 66A>G polymorphism may be associated with OAT risk.


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