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
File Download
(May Require Subscription)
- No File Attached
(May Require Subscription)
- Publisher Website: 10.1016/j.atherosclerosis.2010.07.046
- Scopus: eid_2-s2.0-77958496161
- PMID: 20732682
- Find via
Supplementary
-
Citations:
-
Appears in Collections:
| Title | 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 | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Authors | Xu, M2 4 5 6 Sham, P3 Ye, Z7 Lindpaintner, K1 He, L4 5 6 | ||||||||
| Keywords | Angiotensin II type I receptor gene Coronary heart disease Genetic polymorphism | ||||||||
| Issue Date | 2010 | ||||||||
| Publisher | Elsevier 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?] DOI: http://dx.doi.org/10.1016/j.atherosclerosis.2010.07.046 | ||||||||
| 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. | ||||||||
| ISSN | 0021-9150 2011 Impact Factor: 3.794 2011 SCImago Journal Rankings: 0.372 | ||||||||
| DOI | http://dx.doi.org/10.1016/j.atherosclerosis.2010.07.046 | ||||||||
| ISI Accession Number ID | WOS:000283356400079
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 | References in Scopus |
| dc.contributor.author | Xu, M | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| dc.contributor.author | Sham, P | ||||||||
| dc.contributor.author | Ye, Z | ||||||||
| dc.contributor.author | Lindpaintner, K | ||||||||
| dc.contributor.author | He, L | ||||||||
| dc.date.accessioned | 2011-08-19T07:07:56Z | ||||||||
| dc.date.available | 2011-08-19T07:07:56Z | ||||||||
| dc.date.issued | 2010 | ||||||||
| dc.description.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. | ||||||||
| dc.description.nature | Link_to_subscribed_fulltext | ||||||||
| dc.identifier.citation | Atherosclerosis, 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.citeulike | 7586784 | ||||||||
| dc.identifier.doi | http://dx.doi.org/10.1016/j.atherosclerosis.2010.07.046 | ||||||||
| dc.identifier.epage | 199 | ||||||||
| dc.identifier.hkuros | 189840 | ||||||||
| dc.identifier.isi | WOS:000283356400079
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.issn | 0021-9150 2011 Impact Factor: 3.794 2011 SCImago Journal Rankings: 0.372 | ||||||||
| dc.identifier.issue | 1 | ||||||||
| dc.identifier.openurl | | ||||||||
| dc.identifier.pmid | 20732682 | ||||||||
| dc.identifier.scopus | eid_2-s2.0-77958496161 | ||||||||
| dc.identifier.spage | 191 | ||||||||
| dc.identifier.uri | http://hdl.handle.net/10722/137121 | ||||||||
| dc.identifier.volume | 213 | ||||||||
| dc.language | eng | ||||||||
| dc.publisher | Elsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis | ||||||||
| dc.publisher.place | Ireland | ||||||||
| dc.relation.ispartof | Atherosclerosis | ||||||||
| dc.relation.references | References in Scopus | ||||||||
| dc.subject.mesh | Alleles | ||||||||
| dc.subject.mesh | Coronary Disease - genetics | ||||||||
| dc.subject.mesh | Genetic Predisposition to Disease | ||||||||
| dc.subject.mesh | Genetic Variation | ||||||||
| dc.subject.mesh | Receptor, Angiotensin, Type 1 - genetics | ||||||||
| dc.subject | Angiotensin II type I receptor gene | ||||||||
| dc.subject | Coronary heart disease | ||||||||
| dc.subject | Genetic polymorphism | ||||||||
| dc.title | 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.type | Article |
Author Affiliations
- F. Hoffmann-La Roche AG
- Harvard University
- The University of Hong Kong
- Shanghai Jiaotong University
- Chinese Academy of Sciences
- Fudan University Shanghai Medical College
- University of Cambridge