Evidence map›Paper›PMID 27182613›Full record

ArticleAnatolian journal of cardiology2016

The role of oxidative DNA damage and GSTM1, GSTT1, and hOGG1 gene polymorphisms in coronary artery disease risk.

Ela Kadıoğlu, Gülten Taçoy, Eren Özçağlı, Kaan Okyay, Mehmet K Akboğa, Atiye Çengel, Semra Şardaş

Open access · diamondAbstract read
In one paragraph

Article in Anatolian journal of cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 3 pooled it
1.9field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 3 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. An updated analysis on the association ofThe Journal of international medical research · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Ela KadıoğluDepartment of Toxicology, Faculty of Pharmacy, Gazi University, Ankara-Turkey. ela@gazi.edu.tr.
Gülten TaçoyDepartment of Cardiology, Faculty of Medicine, Gazi University, Ankara-Turkey.
Eren ÖzçağlıDepartment of Toxicology, Faculty of Pharmacy, İstanbul University, İstanbul-Turkey.
Kaan OkyayDepartment of Cardiology, Medical School, Başkent University, Ankara-Turkey.
Mehmet K AkboğaDepartment of Cardiology, Türkiye Yüksek İhtisas Training and Research Hospital, Ankara-Turkey.
Atiye ÇengelDepartment Cardiology, Faculty of Medicine, Gazi University, Ankara-Turkey.
Semra ŞardaşDepartment of Toxicology, Faculty of Pharmacy, Marmara University, İstanbul-Turkey.
Selçuk Üniversitesi Tıp Fakültesi Hastanesi · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAtherosclerotic coronary artery disease (CAD) appears to be a multifactorial process caused by the interaction of environmental risk factors with multiple predisposing genes. Therefore, in this study we aimed to determine the role of oxidative DNA damage and some variations in glutathione S-transferase (GSTM1 and GSTT1) and DNA repair (hOGG1) genes in CAD risk.

methodsA case-control study was conducted on 59 individuals who had undergone coronary angiographic evaluation. Of these, 29 were patients diagnosed with CAD (mean age =61.5±10.3) and 30 were controls examined for reasons other than suspected CAD and who had angiographically documented normal coronary arteries (mean age =60.4±11.6). Basal DNA damage as well as pyrimidine and purine base damage were evaluated in peripheral blood lymphocytes using the modified comet assay. Polymerase chain reaction-restriction length polymorphism (PCR-RFLP)-based assay was used for genotyping.

resultsBasal DNA damage levels in patients [9.16 (3.26)] were significantly higher than those in controls [7.59 (3.23); p=0.017], and basal DNA and pyrimidine base damage levels were significantly correlated with disease severity based on Gensini scoring (r=0.352, p=0.006; r=0.318, p=0.014, respectively). However, no significant differences were observed in terms of oxidized DNA bases between patients and controls. The frequencies of studied genotypes (GSTM1, GSTT1, and hOGG1) were similar between groups.

conclusionThe results of this study pointed out the role of DNA damage in CAD and its severity. However, GSTM1, GSTT1, and hOGG1 gene polymorphisms seemed to have no effect on individual susceptibility for disease progression.

Indexed as

DNA DamageGenetic Predisposition to DiseasePolymorphism, GeneticAdultCase-Control StudiesCoronary Artery DiseaseDNA GlycosylasesFemaleGenotypeGlutathione TransferaseHumansMaleMiddle AgedOxidative StressRisk FactorsDNA Glycosylasesglutathione S-transferase T1Glutathione Transferaseoxoguanine glycosylase 1, human

Identifiers

PMID27182613
PMCPMC5324912
OpenAlexW2342757290

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.