{"title":"Epithelial nitric oxide synthases (eNOS) 894 G < T polymorphism and diabetic nephropathy susceptibility: A meta-analysis","authors":"Hui Li, Guiqin Shu, Huihui Gao","doi":"10.1515/pteridines-2022-0042","DOIUrl":null,"url":null,"abstract":"Abstract Objective To investigate the epithelial nitric oxide synthases (eNOS) 894 G < T polymorphism and diabetic nephropathy (DN) susceptibility by pooling the open published data. Methods Studies relevant to eNOS 894 G < T polymorphism and DN susceptibility published in PubMed, EMBASE, Medline, CNKI, and Wanfang databases were systematically screened by using the text words of endothelial nitric oxide synthase, eNOS, NOS-3, G894T, rs179983, polymorphism, diabetic nephropathy, and DN. The correlation between eNOS 894 G < T polymorphism and DN susceptibility was demonstrated by odds ratio (OR) and corresponding 95% confidence interval (95% CI). The data were combined through fixed or random effect model according to statistical heterogeneity. The publication bias was assessed by Begg’s funnel plot and Egger’s line regression test. Results Twenty-six case-control studies relevant to eNOS 894 G < T polymorphism and DN susceptibility were identified by electronic searching of the related databases. Type 2 diabetes mellitus (T2MD) patients with T allele had increased susceptibility to DN compared with G allele under homologous gene model (TT vs GG) (OR = 1.40, 95% CI: 1.16–1.69, p = 0.001), dominant gene model (TT + GT) vs GG (OR = 1.61, 95% CI: 1.30–2.00, p = 0.000) and recessive gene model TT vs (GT + GG) (OR = 1.39, 95% CI: 1.16–1.66, p = 0.000). Publication bias was not statistically significant for homologous and recessive gene model. Conclusion Based on the present evidence, DN risk was increased in T2MD cases with T allele compared to G allele.","PeriodicalId":20792,"journal":{"name":"Pteridines","volume":"33 1","pages":"49 - 57"},"PeriodicalIF":0.5000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pteridines","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1515/pteridines-2022-0042","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Abstract Objective To investigate the epithelial nitric oxide synthases (eNOS) 894 G < T polymorphism and diabetic nephropathy (DN) susceptibility by pooling the open published data. Methods Studies relevant to eNOS 894 G < T polymorphism and DN susceptibility published in PubMed, EMBASE, Medline, CNKI, and Wanfang databases were systematically screened by using the text words of endothelial nitric oxide synthase, eNOS, NOS-3, G894T, rs179983, polymorphism, diabetic nephropathy, and DN. The correlation between eNOS 894 G < T polymorphism and DN susceptibility was demonstrated by odds ratio (OR) and corresponding 95% confidence interval (95% CI). The data were combined through fixed or random effect model according to statistical heterogeneity. The publication bias was assessed by Begg’s funnel plot and Egger’s line regression test. Results Twenty-six case-control studies relevant to eNOS 894 G < T polymorphism and DN susceptibility were identified by electronic searching of the related databases. Type 2 diabetes mellitus (T2MD) patients with T allele had increased susceptibility to DN compared with G allele under homologous gene model (TT vs GG) (OR = 1.40, 95% CI: 1.16–1.69, p = 0.001), dominant gene model (TT + GT) vs GG (OR = 1.61, 95% CI: 1.30–2.00, p = 0.000) and recessive gene model TT vs (GT + GG) (OR = 1.39, 95% CI: 1.16–1.66, p = 0.000). Publication bias was not statistically significant for homologous and recessive gene model. Conclusion Based on the present evidence, DN risk was increased in T2MD cases with T allele compared to G allele.
期刊介绍:
Pteridines is an open acess international quarterly journal dealing with all aspects of pteridine research. Pteridines are heterocyclic fused ring compounds involved in a wide range of biological functions from the color on butterfly wings to cofactors in enzyme catalysis to essential vitamins. Of the pteridines, 5,6,7,8-tetrahydrobiopterin is the necessary cofactor of several aromatic amino acid monoxygenases, the nitric oxide synthases and glyceryl ether monoxygenase (GEMO). Neopterin plays an essential role in the immune system and is an important biomarker in laboratory medicine for diseases such as HIV, cardiovascular disease, malignant tumors, among others.
Topics:
-Neopterin, dihydroneopterin, monapterin-
Biopterin, tetrahydrobiopterin-
Folates, antifolates, riboflavin-
Phenylalanine, tyrosine, phenylketonuria, serotonin, adrenalin, noradrenalin, L-DOPA, dopamine, related biogenic amines-
Phenylalanine hydroxylase, tyrosine hydroxylase, tryptophan hydroxylase, nitric oxide synthases (iNOS), alkylglycerol monooxygenase (AGMO), dihydropterin reductase, sepiapterin reductase-
Homocysteine, mediators of inflammation, redox systems, iron.