Evidence map›Paper›PMID 26984639›Full record

ArticleScientific reports2016

Associations of functional alanine-glyoxylate aminotransferase 2 gene variants with atrial fibrillation and ischemic stroke.

Ilkka Seppälä, Marcus E Kleber, Steve Bevan, Leo-Pekka Lyytikäinen, Niku Oksala, Jussi A Hernesniemi, Kari-Matti Mäkelä, Peter M Rothwell, Cathie Sudlow, Martin Dichgans and 11 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

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  12. AInternational journal of medical sciences · 2018
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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

21 authors at 14 institutions in 4 countries.

Ilkka SeppäläDepartment of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland.
Marcus E KleberVth Department of Medicine (Nephrology, Hypertensiology, Endocrinology, Diabetology, Rheumatology), Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany.
Steve BevanSchool of Life Science, University of Lincoln, Lincoln, UK.
Leo-Pekka LyytikäinenDepartment of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland.
Niku OksalaDepartment of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland.
Jussi A HernesniemiDepartment of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland.
Kari-Matti MäkeläDepartment of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland.
Peter M RothwellStroke Prevention Research Unit, Nuffield Department of Clinical Neuroscience, University of Oxford, Oxford, UK.
Cathie SudlowDivision of Clinical Neurosciences and Insititute of Genetics and Molecular Medicine, University of Edinburgh, UK.
Martin DichgansInstitute for Stroke and Dementia Research, Klinikum der Universität München, Ludwig-Maximilians-Universität, Munich, Germany &Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.
Nina MononenDepartment of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland.
Efthymia VlachopoulouTransplantation Laboratory, Haartman Institute, University of Helsinki, Helsinki, Finland.
Juha SinisaloHeart and Lung Center, Helsinki University Hospital and Helsinki University, Helsinki, Finland.
Graciela E DelgadoVth Department of Medicine (Nephrology, Hypertensiology, Endocrinology, Diabetology, Rheumatology), Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany.
Reijo LaaksonenDepartment of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland.
Tuomas KoskinenResearch Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland.
Hubert ScharnaglClinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria.
Mika KähönenDepartment of Clinical Physiology, Tampere University Hospital and University of Tampere, Tampere, Finland.
Hugh S MarkusClinical Neurosciences, University of Cambridge, Cambridge, UK.
Winfried MärzVth Department of Medicine (Nephrology, Hypertensiology, Endocrinology, Diabetology, Rheumatology), Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany.
Terho LehtimäkiDepartment of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland.
Fimlab (Finland) · FITampere University · FIHeidelberg University · DEHelsinki University Hospital · FIMedical University of Graz · ATMunich Cluster for Systems Neurology · DETampere University Hospital · FIUniversity Hospital Heidelberg · DEUniversity of Cambridge · GBUniversity of Edinburgh · GBUniversity of Helsinki · FIUniversity of Lincoln · GBUniversity of Oxford · GBUniversity of Turku · FI

Funding

Wellcome Trust 085475/B/08/ZWellcome Trust 085475/Z/08/ZWellcome Trust 095626Wellcome Trust WT084724MA
6 · The paper itself

Abstract

Asymmetric and symmetric dimethylarginines (ADMA and SDMA) impair nitric oxide bioavailability and have been implicated in the pathogenesis of atrial fibrillation (AF). Alanine-glyoxylate aminotransferase 2 (AGXT2) is the only enzyme capable of metabolizing both of the dimethylarginines. We hypothesized that two functional AGXT2 missense variants (rs37369, V140I; rs16899974, V498L) are associated with AF and its cardioembolic complications. Association analyses were conducted using 1,834 individulas with AF and 7,159 unaffected individuals from two coronary angiography cohorts and a cohort comprising patients undergoing clinical exercise testing. In coronary angiography patients without structural heart disease, the minor A allele of rs16899974 was associated with any AF (OR = 2.07, 95% CI 1.59-2.68), and with paroxysmal AF (OR = 1.98, 95% CI 1.44-2.74) and chronic AF (OR = 2.03, 95% CI 1.35-3.06) separately. We could not replicate the association with AF in the other two cohorts. However, the A allele of rs16899974 was nominally associated with ischemic stroke risk in the meta-analysis of WTCCC2 ischemic stroke cohorts (3,548 cases, 5,972 controls) and with earlier onset of first-ever ischemic stroke (360 cases) in the cohort of clinical exercise test patients. In conclusion, AGXT2 variations may be involved in the pathogenesis of AF and its age-related thromboembolic complications.

Indexed as

AgedAllelesAngiographyAtrial FibrillationCase-Control StudiesChronic DiseaseCohort StudiesCoronary VesselsFemaleGenotypeHumansLogistic ModelsMaleMiddle AgedMutation, MissenseOdds RatioAlanine-glyoxylate transaminaseTransaminases

Identifiers

PMID26984639
PMCPMC4794714
OpenAlexW2299514801

What OpenQuestion 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 OpenQuestion graph.