Evidence map›Paper›PMID 12811412›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2003

Interactive effect of the glutathione S-transferase genes and cigarette smoking on occurrence and severity of coronary artery risk.

Serena Masetti, Nicoletta Botto, Samantha Manfredi, Maria Giovanna Colombo, Antonio Rizza, Cristina Vassalle, Aldo Clerico, Andrea Biagini, Maria Grazia Andreassi

Abstract read
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In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 4 pooled it
1.3field-weighted citation impact, top 22% 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

22 citing papers in PubMed, 4 syntheses or guidelines pooled it, 82 citations in OpenAlex.

  1. An updated analysis on the association ofThe Journal of international medical research · 2022
    Pooled it
  2. Pooled it
  3. Association between GSTM1 null genotype and coronary artery disease risk: a meta-analysis.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Pooled it
  4. Pooled it
  5. Review
  6. Association of Glutathione S-TransferaseReports of biochemistry & molecular biology · 2020
    Article
  7. Association ofInternational journal of general medicine · 2020
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Association analysis of GSTT1, GSTM1 genotype polymorphisms and serum total GST activity with ischemic stroke risk.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2010
    Article
  18. Article
  19. Glutathione-S-transferase P protects against endothelial dysfunction induced by exposure to tobacco smoke.American journal of physiology. Heart and circulatory physiology · 2009
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Serena MasettiSant'Anna School, Pisa, Italy.
Nicoletta Botto
Samantha Manfredi
Maria Giovanna Colombo
Antonio Rizza
Cristina Vassalle
Aldo Clerico
Andrea Biagini
Maria Grazia Andreassi
Scan Foundation · USCentro Universitário Sant’Anna · BRScuola Superiore Sant'Anna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular diseases and cancer are the main causes of death in developed countries. Mortality trends for these diseases suggest that they share common pathogenetic mechanisms. Glutathione S-transferase (GST) is a family of enzymes that detoxify reactive electrophiles, particularly present in tobacco smoke. Glutathione S-transferase null M1 and T1 (GSTM1 and GSTT1) genotypes have often been associated with increased risk of developing cancer. Our hypothesis was that the polymorphic GSTM1 and GSTT1 genes modulate the risk of smoking-coronary artery disease (CAD). We evaluated the distribution of GST genotypes in 430 angiographically defined patients (308 CAD and 122 non-CAD). The frequencies of GST null genotypes did not differ significantly between patients with CAD and without CAD. However, smokers with GSTM1 and GSTT1 null genotypes had a significantly higher risk of CAD than never-smokers with these genotypes present (OR 2.2 and 3.4 for smokers with null GSTM1 and GSTT1 genes, respectively). There was also evidence of multiple interaction between GSTM1 and GSTT1 deleted genotypes and smoking. In nonsmokers carrying both null genotypes the risk of CAD was 0.66. In smokers with both present genotypes the OR was 1.5 and was significantly increased in smokers with concurrent lack for GSTM1 and GSTT1 genes (OR=4.0). Moreover, smokers lacking GST genes had both more stenosed vessels and a higher Duke score than smokers expressing the genes. We also examined the levels of DNA damage in 66 men patients using the micronucleus test, a sensitive assay for evaluating chromosome damage. Micronucleus levels were higher in smokers with null genes than in smokers with present genes. These observations suggest that GST-null genotypes strengthen the effect of smoking on CAD risk by modulating the detoxification of genotoxic atherogens.

Indexed as

Coronary Artery DiseaseDisease SusceptibilityFemaleGenetic Predisposition to DiseaseGenetic VariationGenotypeGlutathione TransferaseHumansMaleMicronucleus TestsMiddle AgedOdds RatioPolymorphism, GeneticRisk FactorsSmokingglutathione S-transferase T1Glutathione Transferase

Identifiers

PMID12811412
OpenAlexW2096323559

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.