Evidence mapPaperPMID 23300871Full record

SynthesisPloS one2012

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.

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

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 4 pooled it
1.5field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 4 syntheses or guidelines pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
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  9. Burn injury induces elevated inflammatory traffic: the role of NF-κB.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Review
  10. Metabolic Effects of Oxytocin.Endocrine reviews · 2020
    Review
  11. Article
  12. PPARG2 Pro12Ala and TNFPPAR research · 2019
    Article
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  14. Is the Mouse a Good Model of Human PPARγ-Related Metabolic Diseases?International journal of molecular sciences · 2016
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Zhijun WuDepartment of Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuqing Lou
Wei Jin
Yan Liu
Lin Lu
Guoping Lu
Shanghai Jiao Tong University · CNRuijin Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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, P(heterogeneity) = 0.67, I(2) = 0%) and the homozygote comparison (AlaAla vs ProPro: P = 0.04,OR = 1.30, 95%CI 1.01-1.68, P(heterogeneity) = 0.68, I(2) = 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, P(heterogeneity) = 0.48, I(2) = 0%; AlaAla vs ProPro: P = 0.02,OR = 1.44, 95%CI 1.07-1.93, P(heterogeneity) = 0.46, I(2) = 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, P(heterogeneity) = 0.87,I(2) = 0%) and the homozygote comparison (P = 0.03,OR = 1.83, 95%CI 1.06-3.16, P(heterogeneity) = 0.88, I(2) = 0%). There was no observable publication bias as reflected by funnel plot and Egger's linear regression test (t = -0.12, P = 0.91).

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

Indexed as

Genetic Predisposition to DiseaseAsian PeopleCoronary Artery DiseaseGenotypeHumansPolymorphism, Single NucleotidePPAR gammaRiskWhite PeoplePPAR gamma

Identifiers

PMID23300871
PMCPMC3534032
OpenAlexW2073443819

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.