Endothelial nitric oxide synthase gene polymorphisms and risk of diabetic nephropathy : a systematic review and meta-analysis
Autor(a) principal: | |
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Data de Publicação: | 2014 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/111620 |
Resumo: | Background: Nitric oxide (NO) has numerous functions in the kidney, including control of renal and glomerular hemodynamics, by interfering at multiple pathological and physiologically critical steps of nephron function. Endothelial NOS (eNOS) gene has been considered a potential candidate gene to diabetic nephropathy (DN) susceptibility. Endothelial nitric oxide synthase gene (eNOS-3) polymorphisms have been associated with DN, however some studies do not confirm this association. The analyzed polymorphisms were 4b/4a, T-786C, and G986T. Methods: The Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement was used in this report. Case–control studies that had diabetic patients with DN as cases and diabetic patients without nephropathy as controls, as well as that evaluated at least one of the three polymorphisms of interest were considered eligible. All studies published up until December 31st, 2012 were identified by searching electronic databases. Hardy-Weinberg equilibrium assessment was performed. Gene-disease association was measured using odds ratio estimation based on the following genetic contrast/models: (1) allele contrast; (2) additive model; (3) recessive model; (4) dominant model and (4) co-dominant model. Results: Twenty-two studies were eligible for meta-analysis (4b/a: 15 studies, T-786C: 5 studies, and G984T: 12 studies). Considering 4b/a polymorphism, an association with DN was observed for all genetic models: allele contrast (OR = 1.14, CI: 1.04-1.25); additive (OR = 1.77, CI: 1.37-2.28); recessive (OR = 1.77, CI: 1.38-2,27); dominant (OR = 1.12, CI: 1.01-1.24), with the exception for co-dominance model. As well, T-786C polymorphism showed association with all models, with exception for co-dominance model: allele contrast (OR = 1.22, CI: 1.07-1.39), additive (OR = 1.52, CI: 1.18-1.97), recessive (OR = 1.50, CI: 1.16-1.93), and dominant (OR = 1.11, CI: 1.01-1.23). For the G894T polymorphism, an association with DN was observed in allelic contrast (OR = 1.12, CI: 1.03-1.25) and co-dominance models (OR = 1.13, CI: 1.04-1.37). Conclusions: In the present study, there was association of DN with eNOS 4b/a and T-786C polymorphism, which held in all genetic models tested, except for co-dominance model. G894T polymorphism was associated with DN only in allele contrast and in co-dominance model. This data suggested that the eNOS gene could play a role in the development of DN. |
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Dellaméa, Bruno SchmidtPinto, Lana Catani FerreiraLeitão, Cristiane BauermannSantos, Kátia Gonçalves dosCanani, Luis Henrique Santos2015-03-04T01:58:06Z20141471-2350http://hdl.handle.net/10183/111620000944867Background: Nitric oxide (NO) has numerous functions in the kidney, including control of renal and glomerular hemodynamics, by interfering at multiple pathological and physiologically critical steps of nephron function. Endothelial NOS (eNOS) gene has been considered a potential candidate gene to diabetic nephropathy (DN) susceptibility. Endothelial nitric oxide synthase gene (eNOS-3) polymorphisms have been associated with DN, however some studies do not confirm this association. The analyzed polymorphisms were 4b/4a, T-786C, and G986T. Methods: The Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement was used in this report. Case–control studies that had diabetic patients with DN as cases and diabetic patients without nephropathy as controls, as well as that evaluated at least one of the three polymorphisms of interest were considered eligible. All studies published up until December 31st, 2012 were identified by searching electronic databases. Hardy-Weinberg equilibrium assessment was performed. Gene-disease association was measured using odds ratio estimation based on the following genetic contrast/models: (1) allele contrast; (2) additive model; (3) recessive model; (4) dominant model and (4) co-dominant model. Results: Twenty-two studies were eligible for meta-analysis (4b/a: 15 studies, T-786C: 5 studies, and G984T: 12 studies). Considering 4b/a polymorphism, an association with DN was observed for all genetic models: allele contrast (OR = 1.14, CI: 1.04-1.25); additive (OR = 1.77, CI: 1.37-2.28); recessive (OR = 1.77, CI: 1.38-2,27); dominant (OR = 1.12, CI: 1.01-1.24), with the exception for co-dominance model. As well, T-786C polymorphism showed association with all models, with exception for co-dominance model: allele contrast (OR = 1.22, CI: 1.07-1.39), additive (OR = 1.52, CI: 1.18-1.97), recessive (OR = 1.50, CI: 1.16-1.93), and dominant (OR = 1.11, CI: 1.01-1.23). For the G894T polymorphism, an association with DN was observed in allelic contrast (OR = 1.12, CI: 1.03-1.25) and co-dominance models (OR = 1.13, CI: 1.04-1.37). Conclusions: In the present study, there was association of DN with eNOS 4b/a and T-786C polymorphism, which held in all genetic models tested, except for co-dominance model. G894T polymorphism was associated with DN only in allele contrast and in co-dominance model. This data suggested that the eNOS gene could play a role in the development of DN.application/pdfengBMC medical genetics. London. Vol. 15 (Jan. 2014), p. 9Nefropatias diabéticasPolimorfismo genéticoÓxido nítrico sintase tipo IIIEndothelial nitric oxide synthase gene polymorphisms and risk of diabetic nephropathy : a systematic review and meta-analysisEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSORIGINAL000944867.pdf000944867.pdfTexto completo (inglês)application/pdf1071521http://www.lume.ufrgs.br/bitstream/10183/111620/1/000944867.pdfe081b5b2ae25dc52cb80f31bd00d5448MD51TEXT000944867.pdf.txt000944867.pdf.txtExtracted Texttext/plain44318http://www.lume.ufrgs.br/bitstream/10183/111620/2/000944867.pdf.txtf218e1e0d45b3a913e4c4fb481d1d351MD52THUMBNAIL000944867.pdf.jpg000944867.pdf.jpgGenerated Thumbnailimage/jpeg1810http://www.lume.ufrgs.br/bitstream/10183/111620/3/000944867.pdf.jpgbd2ef424fb13bdc48288ab52bb603a52MD5310183/1116202018-10-24 08:47:14.938oai:www.lume.ufrgs.br:10183/111620Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2018-10-24T11:47:14Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
Endothelial nitric oxide synthase gene polymorphisms and risk of diabetic nephropathy : a systematic review and meta-analysis |
title |
Endothelial nitric oxide synthase gene polymorphisms and risk of diabetic nephropathy : a systematic review and meta-analysis |
spellingShingle |
Endothelial nitric oxide synthase gene polymorphisms and risk of diabetic nephropathy : a systematic review and meta-analysis Dellaméa, Bruno Schmidt Nefropatias diabéticas Polimorfismo genético Óxido nítrico sintase tipo III |
title_short |
Endothelial nitric oxide synthase gene polymorphisms and risk of diabetic nephropathy : a systematic review and meta-analysis |
title_full |
Endothelial nitric oxide synthase gene polymorphisms and risk of diabetic nephropathy : a systematic review and meta-analysis |
title_fullStr |
Endothelial nitric oxide synthase gene polymorphisms and risk of diabetic nephropathy : a systematic review and meta-analysis |
title_full_unstemmed |
Endothelial nitric oxide synthase gene polymorphisms and risk of diabetic nephropathy : a systematic review and meta-analysis |
title_sort |
Endothelial nitric oxide synthase gene polymorphisms and risk of diabetic nephropathy : a systematic review and meta-analysis |
author |
Dellaméa, Bruno Schmidt |
author_facet |
Dellaméa, Bruno Schmidt Pinto, Lana Catani Ferreira Leitão, Cristiane Bauermann Santos, Kátia Gonçalves dos Canani, Luis Henrique Santos |
author_role |
author |
author2 |
Pinto, Lana Catani Ferreira Leitão, Cristiane Bauermann Santos, Kátia Gonçalves dos Canani, Luis Henrique Santos |
author2_role |
author author author author |
dc.contributor.author.fl_str_mv |
Dellaméa, Bruno Schmidt Pinto, Lana Catani Ferreira Leitão, Cristiane Bauermann Santos, Kátia Gonçalves dos Canani, Luis Henrique Santos |
dc.subject.por.fl_str_mv |
Nefropatias diabéticas Polimorfismo genético Óxido nítrico sintase tipo III |
topic |
Nefropatias diabéticas Polimorfismo genético Óxido nítrico sintase tipo III |
description |
Background: Nitric oxide (NO) has numerous functions in the kidney, including control of renal and glomerular hemodynamics, by interfering at multiple pathological and physiologically critical steps of nephron function. Endothelial NOS (eNOS) gene has been considered a potential candidate gene to diabetic nephropathy (DN) susceptibility. Endothelial nitric oxide synthase gene (eNOS-3) polymorphisms have been associated with DN, however some studies do not confirm this association. The analyzed polymorphisms were 4b/4a, T-786C, and G986T. Methods: The Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement was used in this report. Case–control studies that had diabetic patients with DN as cases and diabetic patients without nephropathy as controls, as well as that evaluated at least one of the three polymorphisms of interest were considered eligible. All studies published up until December 31st, 2012 were identified by searching electronic databases. Hardy-Weinberg equilibrium assessment was performed. Gene-disease association was measured using odds ratio estimation based on the following genetic contrast/models: (1) allele contrast; (2) additive model; (3) recessive model; (4) dominant model and (4) co-dominant model. Results: Twenty-two studies were eligible for meta-analysis (4b/a: 15 studies, T-786C: 5 studies, and G984T: 12 studies). Considering 4b/a polymorphism, an association with DN was observed for all genetic models: allele contrast (OR = 1.14, CI: 1.04-1.25); additive (OR = 1.77, CI: 1.37-2.28); recessive (OR = 1.77, CI: 1.38-2,27); dominant (OR = 1.12, CI: 1.01-1.24), with the exception for co-dominance model. As well, T-786C polymorphism showed association with all models, with exception for co-dominance model: allele contrast (OR = 1.22, CI: 1.07-1.39), additive (OR = 1.52, CI: 1.18-1.97), recessive (OR = 1.50, CI: 1.16-1.93), and dominant (OR = 1.11, CI: 1.01-1.23). For the G894T polymorphism, an association with DN was observed in allelic contrast (OR = 1.12, CI: 1.03-1.25) and co-dominance models (OR = 1.13, CI: 1.04-1.37). Conclusions: In the present study, there was association of DN with eNOS 4b/a and T-786C polymorphism, which held in all genetic models tested, except for co-dominance model. G894T polymorphism was associated with DN only in allele contrast and in co-dominance model. This data suggested that the eNOS gene could play a role in the development of DN. |
publishDate |
2014 |
dc.date.issued.fl_str_mv |
2014 |
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2015-03-04T01:58:06Z |
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000944867 |
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BMC medical genetics. London. Vol. 15 (Jan. 2014), p. 9 |
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