Evidence map›Paper›PMID 30188935›Full record

ArticlePloS one2018

Associations and interactions between variants in selenoprotein genes, selenoprotein levels and the development of abdominal aortic aneurysm, peripheral arterial disease, and heart failure.

Ewa Strauss, Jolanta Tomczak, Ryszard Staniszewski, Grzegorz Oszkinis

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
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

16 citing papers in PubMed, 27 citations in OpenAlex.

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  8. Lower Plasma Selenoprotein P Levels in Regularly Exercising Young Adults.Journal of the ASEAN Federation of Endocrine Societies · 2023
    Article
  9. Review
  10. Selenoprotein S: A versatile disordered protein.Archives of biochemistry and biophysics · 2022
    Review
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  12. Article
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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

4 authors at 1 institution in 1 country.

Ewa StraussInstitute of Human Genetics, Polish Academy of Sciences, Poznan, Poland.ORCID 0000-0001-8275-3126
Jolanta TomczakDepartment of General and Vascular Surgery, Poznan University of Medical Sciences, Poznan, Poland.
Ryszard StaniszewskiDepartment of Vascular and Endovascular Surgery, Angiology and Phlebology, Poznan University of Medical Sciences, Poznan, Poland.
Grzegorz OszkinisDepartment of General and Vascular Surgery, Poznan University of Medical Sciences, Poznan, Poland.
Poznan University of Medical Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLittle is known on the role of selenoprotein genes in cardiovascular disease. This study examines the associations of the SEPP1, SELENOS, TXNRD1, TXNRD2, GPX4, and SOD2 polymorphisms and selenoprotein P (SeP) and thioredoxin concentrations with the development of abdominal aortic aneurysm (AAA) and aortoiliac occlusive disease (AOID), as well as their influence on cardiac phenotype.

methods564 patients with AAA, 400 patients with AIOD, and 543 controls were enrolled and characterized for coronary artery disease, myocardial infarction, and systolic heart failure (HF) occurrence. In AAA, the coexistence of peripheral arterial disease (PAD) was examined. Genotypes were determined using TaqMan-based assays. Selenoprotein concentration was assessed using the ELISA method.

resultsThe SELENOS rs34713741T, SEPP1 rs3877899A, and GPX4 rs713041T alleles were related to a 30-60% increase in the AIOD/PAD risk in the recessive or dominant model (all associations at P < .05). The SEPP1 rs3877899A allele was a protective factor for the development of AAA without concomitant PAD (OR = 0.68 for the dominant model, P = .014), but not AAA with concomitant PAD. The cumulative two-locus effects of selenoprotein genes on the AAA/AIOD risk were observed, including the multiplicative interaction between the SELENOS rs34713741T and GPX4 rs713041T alleles (both in the recessive model) affecting the AIOD risk (OR = 5.27, P = .001) and its clinical phenotype. Coexistence of HF in aortic diseases was related to both the SEPP1 rs7579A allele (OR = 1.83 for carriers, P = .013) and increased SeP concentrations; SeP level ≥8.5 mg/mL caused a 3.5-fold increase in the risk of HF. In AAA, SeP levels were correlated with BMI (r = -0.575, P < .0001).

conclusionsOur results provide evidence that selenoprotein polymorphisms constitute a risk factor for HF and peripheral atherosclerosis, but prevent the development of AAA. Excessive weight might result in reduced antioxidant reserve efficiency in AAA. Validation studies are required to establish whether SeP concentration may be a marker for HF.

Indexed as

AgedAged, 80 and overAortic Aneurysm, AbdominalCase-Control StudiesFemaleGenetic Association StudiesGenetic Predisposition to DiseaseGlutathione PeroxidaseHeart FailureHumansMaleMembrane ProteinsMiddle AgedPeripheral Arterial DiseasePhospholipid Hydroperoxide Glutathione PeroxidasePolymorphism, Single NucleotideGlutathione PeroxidaseMembrane ProteinsPhospholipid Hydroperoxide Glutathione PeroxidaseSELENOP protein, humanSelenoprotein PSelenoproteinsSELENOS protein, human

Identifiers

PMID30188935
PMCPMC6126836
OpenAlexW2891998808

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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.