PPARgamma Promoter Polymorphisms and Acute Coronary Syndrome

Evangelisti, L; Attanasio, Monica; Lucarini, Laura; Sofi, Francesco; Marcucci, Rossella; Giglioli, Cristina; Valente, Serafina; Gensini, Gianfranco; Abbate, Rosanna; Pepe, Guglielmina

doi:10.1016/j.atherosclerosis.2008.11.009

Cited by 23 publications

(21 citation statements)

References 36 publications

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“…8 of the 22 qualified studies were prospective [22], [36], [43], [44], [53], [54] and the others were retrospective. 11 studies were population-based (P–B) [22], [36], [44], [47], [49], [50], [52]–[54] and the rest half were hospital-based (H–B). 15 studies were analyzed for CAD [22], [36], [42], [43], [47], [48], [50], [51], [54] as the primary outcome, 2 studies for ACS [49], [53] and 5 studies for MI [18], [21], [23], [44], [52] as an end point.…”

Section: Resultsmentioning

confidence: 99%

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

Lou

Jin

et al. 2012

PLoS ONE

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BackgroundContradictory 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.MethodsStudies 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.ResultsThe 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.

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Section: Resultsmentioning

confidence: 99%

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

Lou

Jin

et al. 2012

PLoS ONE

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“…We next created a Galbraith plot to graphically assess the source of the heterogeneity. As a result, five studies 15,28,32,34,37) were identified as the main contributors of heterogeneity for the allelic models, two studies 15,37) were identified as the main contributors of heterogeneity for the additive and recessive models and four studies 11,28,32,37) were identified as contributors of heterogeneity for the dominant model (Fig. 7).…”

Section: Discussionmentioning

confidence: 99%

Association between Peroxisome Proliferator-activated Receptor Gamma Gene Polymorphisms and Atherosclerotic Diseases: A Meta-analysis of Case-control Studies

Wang

Yin

et al. 2015

JAT

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Aim:The aim of this study was to perform a meta-analysis to investigate the association between PPAR rs1801282/rs3856806 polymorphisms and atherosclerotic diseases. Methods: The meta-analysis was performed by searching the PubMed, Embase and Web of Science databases from the first available year to September 10, 2013. Additionally, reference lists from the identified articles, reviews and abstracts presented at the meetings of related scientific societies were also checked. All case-control studies investigating the association between PPAR rs1801282/ rs3856806 polymorphisms and the risk of atherosclerotic disease were included. The association was assessed according to the odds ratio (OR) with a 95% confidence interval (CI). Publication bias was analyzed using Begg's funnel plot and Egger's regression test. Results: A total of 29 studies reporting PPAR rs1801282/rs3856806 polymorphism were included in the final meta-analysis. Neither the rs1801282 (Pro12Ala) nor rs3856806 (C161T) polymorphisms showed any significant associations with susceptibility to atherosclerotic diseases. In the meta-analysis performed to assess the association between the rs3856806 gene polymorphism and atherosclerotic disease based on ethnicity and the type of disease, significant associations were found in the Caucasian subgroup, Asian, CAD and MI subgroups. Conclusions: The present data suggest that there is no statistical evidence of a significant association between the PPAR gene rs1801282/rs3856806 polymorphism and the risk of atherosclerotic disease. In contrast, the rs3856806 polymorphism was associated with an increased risk in the Caucasian and MI subgroups, whereas decreased risks were noted in the Asian and CAD subgroups. Due to significant between-study heterogeneity, further studies with a larger sample size involving homogeneous AS patients and well-matched controls are required in the future.

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“…The phenotype of this SNP was weakening with the presence of P12P homozygote genotype [46]. Moreover, in an Italian cohort, the 93695C > T PPARγ promoter polymorphism was found to have a protective role in acute coronary syndrome [56]. Furthermore, the C1431T PPARγ polymorphism was associated not only with altered plasma lipids during fasting but also with higher risk of an angiography defined CVD [47].…”

Section: Human Aspects Of Pparγ In Metabolic Syndromementioning

confidence: 99%

Is the Mouse a Good Model of Human PPARγ-Related Metabolic Diseases?

Pap

Cuaranta-Monroy

Peloquin

et al. 2016

IJMS

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With the increasing number of patients affected with metabolic diseases such as type 2 diabetes, obesity, atherosclerosis and insulin resistance, academic researchers and pharmaceutical companies are eager to better understand metabolic syndrome and develop new drugs for its treatment. Many studies have focused on the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), which plays a crucial role in adipogenesis and lipid metabolism. These studies have been able to connect this transcription factor to several human metabolic diseases. Due to obvious limitations concerning experimentation in humans, animal models—mainly mouse models—have been generated to investigate the role of PPARγ in different tissues. This review focuses on the metabolic features of human and mouse PPARγ-related diseases and the utility of the mouse as a model.

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PPARgamma Promoter Polymorphisms and Acute Coronary Syndrome

Abstract: The protective role of 93695C>T polymorphism in PPARg promoter in ACS suggests that PPARg genetic variants may affect the susceptibility to atherosclerotic diseases.

Cited by 23 publications

References 36 publications

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

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

Association between Peroxisome Proliferator-activated Receptor Gamma Gene Polymorphisms and Atherosclerotic Diseases: A Meta-analysis of Case-control Studies

Is the Mouse a Good Model of Human PPARγ-Related Metabolic Diseases?

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