The Pro12Ala Polymorphism in the Peroxisome Proliferator-Activated Receptor Gamma-2 Gene PPARγ2 Is Associated with Increased Risk of Coronary Artery Disease: A Meta-AnalysisReportar como inadecuado




The Pro12Ala Polymorphism in the Peroxisome Proliferator-Activated Receptor Gamma-2 Gene PPARγ2 Is Associated with Increased Risk of Coronary Artery Disease: A Meta-Analysis - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Background

Contradictory results have been reported regarding the association between Pro12Ala polymorphism of PPARγ2 and coronary artery disease CAD. We sought to estimate the inconsistent results by performing a comprehensive meta-analysis.

Methods

Studies in English or Chinese publications were identified by screening MEDLINE, Embase, CNKI, Wanfang and CBM. 22 studies including 8948 cases and 14427 controls were selected. A random-effects model was applied to combine the divergent outcomes of the individual studies, while addressing between-study heterogeneity and publication bias.

Results

The Pro12Ala polymorphism of control population followed Hardy-Weinberg equilibrium for all studies P>0.05. Overall, a marginal increased risk of CAD under the recessive genetic model AlaAla vs ProAla+ProPro: P = 0.04, OR = 1.31, 95%CI 1.01–1.69, Pheterogeneity = 0.67, I2 = 0% and the homozygote comparison AlaAla vs ProPro: P = 0.04,OR = 1.30, 95%CI 1.01–1.68, Pheterogeneity = 0.68, I2 = 0% was observed. In the subgroup analysis by ethnicity, carriers of AlaAla homozygotes had a significant increased risk for CAD among Caucasians AlaAla vs ProAla+ProPro: P = 0.01, OR = 1.45, 95%CI 1.08–1.96, Pheterogeneity = 0.48, I2 = 0%; AlaAla vs ProPro: P = 0.02,OR = 1.44, 95%CI 1.07–1.93, Pheterogeneity = 0.46, I2 = 0%. After dividing into population source, the CAD risk magnitude of hospital-based studies was distinctly strengthened under the recessive model P = 0.03,OR = 1.85,95%CI 1.07–3.19, Pheterogeneity = 0.87,I2 = 0% and the homozygote comparison P = 0.03,OR = 1.83, 95%CI 1.06–3.16, Pheterogeneity = 0.88, I2 = 0%. There was no observable publication bias as reflected by funnel plot and Egger’s linear regression test t = -0.12, P = 0.91.

Conclusion:

Our results demonstrated that the PPARγ2 Pro12Ala polymorphism might be risk-conferring locus for the progression of CAD among Caucasians, but not among Asians.



Autor: Zhijun Wu , Yuqing Lou , Wei Jin, Yan Liu, Lin Lu, Guoping Lu

Fuente: http://plos.srce.hr/



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