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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

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
Authors
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
Citation
Atherosclerosis, 2010, v. 213 n. 1, p. 191-199 How to Cite?
Abstract
Objective: 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.
Persistent Identifierhttp://hdl.handle.net/10722/137121
ISSN
2013 Impact Factor: 3.971
2013 SCImago Journal Rankings: 1.728
ISI Accession Number ID
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.

References

 

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
DC FieldValueLanguage
dc.contributor.authorXu, Men_HK
dc.contributor.authorSham, Pen_HK
dc.contributor.authorYe, Zen_HK
dc.contributor.authorLindpaintner, Ken_HK
dc.contributor.authorHe, Len_HK
dc.date.accessioned2011-08-19T07:07:56Z-
dc.date.available2011-08-19T07:07:56Z-
dc.date.issued2010en_HK
dc.identifier.citationAtherosclerosis, 2010, v. 213 n. 1, p. 191-199en_HK
dc.identifier.issn0021-9150en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137121-
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.en_HK
dc.languageeng-
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosisen_HK
dc.relation.ispartofAtherosclerosisen_HK
dc.subjectAngiotensin II type I receptor geneen_HK
dc.subjectCoronary heart diseaseen_HK
dc.subjectGenetic polymorphismen_HK
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.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 controlsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9150&volume=213&issue=1&spage=191&epage=199&date=2010&atitle=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-
dc.identifier.emailSham, P: pcsham@hku.hken_HK
dc.identifier.authoritySham, P=rp00459en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.atherosclerosis.2010.07.046en_HK
dc.identifier.pmid20732682en_HK
dc.identifier.scopuseid_2-s2.0-77958496161en_HK
dc.identifier.hkuros189840-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77958496161&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume213en_HK
dc.identifier.issue1en_HK
dc.identifier.spage191en_HK
dc.identifier.epage199en_HK
dc.identifier.isiWOS:000283356400079-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridXu, M=7403607565en_HK
dc.identifier.scopusauthoridSham, P=34573429300en_HK
dc.identifier.scopusauthoridYe, Z=7401956870en_HK
dc.identifier.scopusauthoridLindpaintner, K=18335428900en_HK
dc.identifier.scopusauthoridHe, L=36080215400en_HK
dc.identifier.citeulike7586784-

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