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Article: A1166C genetic variation of the angiotensin II type I receptor gene and susceptibility to coronary heart disease: Collaborative of 53 studies with 20,435 cases and 23,674 controls
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TitleA1166C genetic variation of the angiotensin II type I receptor gene and susceptibility to coronary heart disease: Collaborative of 53 studies with 20,435 cases and 23,674 controls
 
AuthorsXu, M6 5 2 4
Sham, P3
Ye, Z7
Lindpaintner, K1
He, L6 5 4
 
KeywordsAngiotensin II type I receptor gene
Coronary heart disease
Genetic polymorphism
 
Issue Date2010
 
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis
 
CitationAtherosclerosis, 2010, v. 213 n. 1, p. 191-199 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.atherosclerosis.2010.07.046
 
AbstractObjective: Angiotensin II induces vasoconstriction and vascular smooth muscle growth via stimulation of the angiotensin II type I receptor (AGTR1). Some studies have reported an association between a genetic variant (A1166C) in the 3' un-translated region of AGTR1 and increased risk of coronary heart disease (CHD), but other have yielded apparently conflicting results. Methods: Literature-based meta-analyses were performed on 48 papers including 53 studies published before June 2008 in relation to the A1166C polymorphism (NCBI, dbSNP: rs5186) of the AGTR1, involving a total of 20,435 CHD cases and 23,674 controls. We also explored potential sources of heterogeneity and conducted appropriate stratified analyses. Results: In a combined analysis, the per-allele odds ratio (OR) for CHD of the A1166C polymorphism was 1.11 (95% confidence interval: 1.03-1.19), but there is an indication of publication bias and heterogeneity among the 53 studies. Sample size and study quality were significant sources of heterogeneity among studies of the A1166C polymorphism with possibly overestimates in studies of smaller sample-size and poor-quality. When the analyses were restricted to 11 larger studies (≥500 cases), and to 8 high-quality studies (quality score: ≥11 points), the summary per-allele odds ratios were 0.992 (95% confidence interval, 0.944-1.042) and 0.990 (95% confidence interval, 0.915-1.072), respectively. Conclusions: An overall weak association between the A1166C polymorphism and CHD is observed but this is likely to be due to publication bias and heterogeneity between studies. There were no significant associations among the larger sample-size and high-quality studies which are less prone to selective publication and have greater power to detect a true association. © 2010 Elsevier Ireland Ltd.
 
ISSN0021-9150
2013 Impact Factor: 3.971
2013 SCImago Journal Rankings: 1.728
 
DOIhttp://dx.doi.org/10.1016/j.atherosclerosis.2010.07.046
 
ISI Accession Number IDWOS:000283356400079
Funding AgencyGrant Number
973 Program2010CB529600
2007CB947300
2006CB910601
863 Program2006AA02A407
2009AA022701
Shanghai Municipal Commission of Science and Technology09DJ1400601
Funding Information:

This work was supported by the 973 Program (2010CB529600, 2007CB947300, 2006CB910601), the 863 Program (2006AA02A407, 2009AA022701), the Shanghai Municipal Commission of Science and Technology Program (09DJ1400601). We sincerely thank Prof. Alessandro Doria from Harvard Medical School and Joslin Diabetes Center for his helpful suggestions on an earlier draft of the paper.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorXu, M
 
dc.contributor.authorSham, P
 
dc.contributor.authorYe, Z
 
dc.contributor.authorLindpaintner, K
 
dc.contributor.authorHe, L
 
dc.date.accessioned2011-08-19T07:07:56Z
 
dc.date.available2011-08-19T07:07:56Z
 
dc.date.issued2010
 
dc.description.abstractObjective: Angiotensin II induces vasoconstriction and vascular smooth muscle growth via stimulation of the angiotensin II type I receptor (AGTR1). Some studies have reported an association between a genetic variant (A1166C) in the 3' un-translated region of AGTR1 and increased risk of coronary heart disease (CHD), but other have yielded apparently conflicting results. Methods: Literature-based meta-analyses were performed on 48 papers including 53 studies published before June 2008 in relation to the A1166C polymorphism (NCBI, dbSNP: rs5186) of the AGTR1, involving a total of 20,435 CHD cases and 23,674 controls. We also explored potential sources of heterogeneity and conducted appropriate stratified analyses. Results: In a combined analysis, the per-allele odds ratio (OR) for CHD of the A1166C polymorphism was 1.11 (95% confidence interval: 1.03-1.19), but there is an indication of publication bias and heterogeneity among the 53 studies. Sample size and study quality were significant sources of heterogeneity among studies of the A1166C polymorphism with possibly overestimates in studies of smaller sample-size and poor-quality. When the analyses were restricted to 11 larger studies (≥500 cases), and to 8 high-quality studies (quality score: ≥11 points), the summary per-allele odds ratios were 0.992 (95% confidence interval, 0.944-1.042) and 0.990 (95% confidence interval, 0.915-1.072), respectively. Conclusions: An overall weak association between the A1166C polymorphism and CHD is observed but this is likely to be due to publication bias and heterogeneity between studies. There were no significant associations among the larger sample-size and high-quality studies which are less prone to selective publication and have greater power to detect a true association. © 2010 Elsevier Ireland Ltd.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationAtherosclerosis, 2010, v. 213 n. 1, p. 191-199 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.atherosclerosis.2010.07.046
 
dc.identifier.citeulike7586784
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.atherosclerosis.2010.07.046
 
dc.identifier.epage199
 
dc.identifier.hkuros189840
 
dc.identifier.isiWOS:000283356400079
Funding AgencyGrant Number
973 Program2010CB529600
2007CB947300
2006CB910601
863 Program2006AA02A407
2009AA022701
Shanghai Municipal Commission of Science and Technology09DJ1400601
Funding Information:

This work was supported by the 973 Program (2010CB529600, 2007CB947300, 2006CB910601), the 863 Program (2006AA02A407, 2009AA022701), the Shanghai Municipal Commission of Science and Technology Program (09DJ1400601). We sincerely thank Prof. Alessandro Doria from Harvard Medical School and Joslin Diabetes Center for his helpful suggestions on an earlier draft of the paper.

 
dc.identifier.issn0021-9150
2013 Impact Factor: 3.971
2013 SCImago Journal Rankings: 1.728
 
dc.identifier.issue1
 
dc.identifier.openurl
 
dc.identifier.pmid20732682
 
dc.identifier.scopuseid_2-s2.0-77958496161
 
dc.identifier.spage191
 
dc.identifier.urihttp://hdl.handle.net/10722/137121
 
dc.identifier.volume213
 
dc.languageeng
 
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis
 
dc.publisher.placeIreland
 
dc.relation.ispartofAtherosclerosis
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAlleles
 
dc.subject.meshCoronary Disease - genetics
 
dc.subject.meshGenetic Predisposition to Disease
 
dc.subject.meshGenetic Variation
 
dc.subject.meshReceptor, Angiotensin, Type 1 - genetics
 
dc.subjectAngiotensin II type I receptor gene
 
dc.subjectCoronary heart disease
 
dc.subjectGenetic polymorphism
 
dc.titleA1166C genetic variation of the angiotensin II type I receptor gene and susceptibility to coronary heart disease: Collaborative of 53 studies with 20,435 cases and 23,674 controls
 
dc.typeArticle
 
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Author Affiliations
  1. F. Hoffmann-La Roche AG
  2. Harvard University
  3. The University of Hong Kong
  4. Shanghai Jiaotong University
  5. Chinese Academy of Sciences
  6. Fudan University Shanghai Medical College
  7. University of Cambridge