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Article: Three endothelial nitric oxide (NOS3) gene polymorphisms in hypertensive and normotensive individuals: Meta-analysis of 53 studies reveals evidence of publication bias

TitleThree endothelial nitric oxide (NOS3) gene polymorphisms in hypertensive and normotensive individuals: Meta-analysis of 53 studies reveals evidence of publication bias
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2007
PublisherLippincott Williams & Wilkins, Ltd. The Journal's web site is located at http://www.jhypertension.com/
Citation
Journal Of Hypertension, 2007, v. 25 n. 9, p. 1763-1774 How to Cite?
AbstractBACKGROUND: Studies on the relationship between endothelial nitric oxide (NOS3) gene variants and hypertension have been conflicting. To explore this hypothesis further, we performed a meta-analysis and re-evaluated the relationship between the three most widely studied NOS3 polymorphisms and hypertension status and blood pressure levels. METHODS: Data on 40 413 subjects from 53 studies were combined in five distinct meta-analyses, and heterogeneity and publication bias were explored. RESULTS: Heterogeneity was observed in all meta-analyses. By a random-effects model, carriers of the four 27-basepair repeat variable number of tandem repeats in intron 4 were associated with a 28% increase in the risk of hypertension compared with those homozygous for the 5 repeat: odds ratio (OR) 1.28, 95% confidence interval (CI) 1.11-1.47, P = 0.001. In Asian individuals, Asp allele carriers displayed a similar association: OR 1.28, 95% CI 1.06-1.54, P = 0.01, as well as a 2 mmHg increase in both systolic (P = 0.04) and diastolic (P = 0.009) blood pressure levels. Furthermore, meta-regression analysis indicated that the effect of the Glu298Asp genotype on the risk of hypertension might be dependent on total cholesterol status. No effect of the T-786C variant on hypertension was detected. There was evidence that such findings might be a result of selectively reporting/publishing positive reports. CONCLUSION: Our results suggest that current data on the relationship between NOS3 variants and hypertension are subject not only to important heterogeneity but also to publication bias. Future research should preferentially focus on gene-environment interactions as well as haplotype analyses. © 2007 Lippincott Williams & Wilkins, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/91489
ISSN
2015 Impact Factor: 5.062
2015 SCImago Journal Rankings: 2.193
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPereira, TVen_HK
dc.contributor.authorRudnicki, Men_HK
dc.contributor.authorCheung, BMYen_HK
dc.contributor.authorBaum, Len_HK
dc.contributor.authorYamada, Yen_HK
dc.contributor.authorOliveira, PSLen_HK
dc.contributor.authorPereira, ACen_HK
dc.contributor.authorKrieger, JEen_HK
dc.date.accessioned2010-09-17T10:20:14Z-
dc.date.available2010-09-17T10:20:14Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of Hypertension, 2007, v. 25 n. 9, p. 1763-1774en_HK
dc.identifier.issn0263-6352en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91489-
dc.description.abstractBACKGROUND: Studies on the relationship between endothelial nitric oxide (NOS3) gene variants and hypertension have been conflicting. To explore this hypothesis further, we performed a meta-analysis and re-evaluated the relationship between the three most widely studied NOS3 polymorphisms and hypertension status and blood pressure levels. METHODS: Data on 40 413 subjects from 53 studies were combined in five distinct meta-analyses, and heterogeneity and publication bias were explored. RESULTS: Heterogeneity was observed in all meta-analyses. By a random-effects model, carriers of the four 27-basepair repeat variable number of tandem repeats in intron 4 were associated with a 28% increase in the risk of hypertension compared with those homozygous for the 5 repeat: odds ratio (OR) 1.28, 95% confidence interval (CI) 1.11-1.47, P = 0.001. In Asian individuals, Asp allele carriers displayed a similar association: OR 1.28, 95% CI 1.06-1.54, P = 0.01, as well as a 2 mmHg increase in both systolic (P = 0.04) and diastolic (P = 0.009) blood pressure levels. Furthermore, meta-regression analysis indicated that the effect of the Glu298Asp genotype on the risk of hypertension might be dependent on total cholesterol status. No effect of the T-786C variant on hypertension was detected. There was evidence that such findings might be a result of selectively reporting/publishing positive reports. CONCLUSION: Our results suggest that current data on the relationship between NOS3 variants and hypertension are subject not only to important heterogeneity but also to publication bias. Future research should preferentially focus on gene-environment interactions as well as haplotype analyses. © 2007 Lippincott Williams & Wilkins, Inc.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins, Ltd. The Journal's web site is located at http://www.jhypertension.com/en_HK
dc.relation.ispartofJournal of Hypertensionen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.subject.meshAllelesen_HK
dc.subject.meshBlood Pressureen_HK
dc.subject.meshGenetic Heterogeneityen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHypertension - enzymology - genetics - physiopathologyen_HK
dc.subject.meshNitric Oxide Synthase Type III - geneticsen_HK
dc.subject.meshPolymorphism, Geneticen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.subject.meshPublication Biasen_HK
dc.subject.meshRisk Factorsen_HK
dc.titleThree endothelial nitric oxide (NOS3) gene polymorphisms in hypertensive and normotensive individuals: Meta-analysis of 53 studies reveals evidence of publication biasen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, BMY:mycheung@hku.hken_HK
dc.identifier.authorityCheung, BMY=rp01321en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/HJH.0b013e3281de740den_HK
dc.identifier.pmid17762636-
dc.identifier.scopuseid_2-s2.0-34548385729en_HK
dc.identifier.hkuros180160-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34548385729&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1763en_HK
dc.identifier.epage1774en_HK
dc.identifier.isiWOS:000249054300002-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridPereira, TV=13405714800en_HK
dc.identifier.scopusauthoridRudnicki, M=15019830600en_HK
dc.identifier.scopusauthoridCheung, BMY=7103294806en_HK
dc.identifier.scopusauthoridBaum, L=7103310839en_HK
dc.identifier.scopusauthoridYamada, Y=7407166277en_HK
dc.identifier.scopusauthoridOliveira, PSL=35389514400en_HK
dc.identifier.scopusauthoridPereira, AC=7402230187en_HK
dc.identifier.scopusauthoridKrieger, JE=7201508348en_HK

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