Evidence map›Paper›PMID 27067415›Full record

ArticleBiological research2016

MnSOD and GPx1 polymorphism relationship with coronary heart disease risk and severity.

Yosra Souiden, Hela Mallouli, Salah Meskhi, Yassine Chaabouni, Ahmed Rebai, Foued Chéour, Kacem Mahdouani

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  8. The Association Between Antioxidant Enzyme Polymorphisms with Type 2 Diabetes Mellitus in Jazan Province.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
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  11. The ALA5/ALA6/ALA7 repeat polymorphisms of the glutathione peroxidase-1 (GPx1) gene and autism spectrum disorder.Autism research : official journal of the International Society for Autism Research · 2022
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  18. International journal of medical sciences · 2019
    Observational
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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

7 authors at 4 institutions in 1 country.

Yosra SouidenLaboratory of Biochemistry and Molecular Biology, Hospital of Ibn Eljazzar of Kairouan, Avenue Ibn Eljazzar, 3140, Kairouan, Tunisia. molbiol_kair@yahoo.fr.
Hela MallouliLaboratory of Biochemistry and Molecular Biology, Hospital of Ibn Eljazzar of Kairouan, Avenue Ibn Eljazzar, 3140, Kairouan, Tunisia.
Salah MeskhiDepartment of Cardiovascular, Hospital of Ibn Eljazzar of Kairouan, Avenue Ibn Eljazzar, 3140, Kairouan, Tunisia.
Yassine ChaabouniLaboratory of Biochemistry and Molecular Biology, Hospital of Ibn Eljazzar of Kairouan, Avenue Ibn Eljazzar, 3140, Kairouan, Tunisia.
Ahmed RebaiLaboratory of Molecular and Cellular Screening Processes, Center of Biotechnology of Sfax, P. O. Box 1177, 3018, Sfax, Tunisia.
Foued ChéourInstitute of Applied Biology of Medenine, 4119, Medenine, Tunisia.
Kacem MahdouaniLaboratory of Biochemistry and Molecular Biology, Hospital of Ibn Eljazzar of Kairouan, Avenue Ibn Eljazzar, 3140, Kairouan, Tunisia.
University of Kairouan · TNCentre of Biotechnology of Sfax · TNInstitut des Régions Arides · TNUniversity of Monastir · TN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDisturbance of the equilibrium between reactive oxygen species (ROS) and anti-oxidants (AOX) has been implicated in various diseases, including atherosclerosis, the most common pathologic process underlying coronary heart disease (CHD). Thus, the defense systems against ROS are critical protecting blood vessel walls against oxidative damage. In this study, we investigate whether Ala16Val MnSOD and Pro198Leu GPx polymorphisms are associated with CHD susceptibility and/or severity.

methodsBoth polymorphisms were genotyped in a sample of 203 controls and 164 patients. CHD risk and severity, antioxidant status (enzymatic and/or non enzymatic) and biochemical parameters were assessed and analysed by genotype.

resultsA significant association of MnSOD variant to CHD risk was revealed in males. Males harboring the Val/Val genotype were approximately at twofold increased risk of CHD compared to controls (Ala carriers vs Val/Val, adjusted OR 1.89; 95 % CI 1.18‒3.42, p = 0.03). Significant decreases in SOD activity and total antioxidant status (TAS) were observed in Val carriers and by CHD status. Whereas, no association of GPx variant genotype (Leu/Leu) and activity to cardiopathy events was discerned. CHD severity, as demonstrated by the number of vessel stenosis, was associated with significantly higher frequency of Val allele and LDL levels in CHD subjects.

conclusionsOur results showed a lack of association of Pro198Leu GPx polymorphism to CHD risk and severity. However, they suggest that Ala16Val MnSOD polymorphism and decreased antioxidant defences are likely contributed to CHD risk in Tunisian men. Furthermore, the Val encoding MnSOD allele and decreased SOD activity were significantly correlated with CHD stenosis progression.

Indexed as

Polymorphism, GeneticAdultAgedAnalysis of VarianceCase-Control StudiesCoronary DiseaseFemaleGenotypeGlutathione PeroxidaseGlutathione Peroxidase GPX1HumansMaleMiddle AgedOxidative StressPolymerase Chain ReactionRisk AssessmentGlutathione PeroxidaseGlutathione Peroxidase GPX1GPX1 protein, humanSuperoxide DismutaseAtherosclerosisCoronary heart diseaseGenetic polymorphismGPx activitySOD activityTotal antioxidant status

Identifiers

PMID27067415
PMCPMC4828869
OpenAlexW2333888269

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Registered trials

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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.