Evidence map›Paper›PMID 20145677›Full record

ArticleEuropean journal of human genetics : EJHG2010

Evidence for CTLA4 as a susceptibility gene for dilated cardiomyopathy.

Volker Ruppert, Thomas Meyer, Clarissa Struwe, Jana Petersen, Andreas Perrot, Maximilian G Posch, Cemil Ozcelik, Anette Richter, Bernhard Maisch, Sabine Pankuweit and 1 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03090425 (Inflammatory/Familial Dilated Cardiomyopathy), which is not on this map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.2field-weighted citation impact, top 38% 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.

NCT03090425 completednot on this mapstarted 2016, after this paper: background citation

Inflammatory/Familial Dilated Cardiomyopathy: Is There a Link to Autoimmune Diseases? TP9a of the KNHI Associated to the DZHK

TypeobservationalSponsorPhilipps University MarburgRan2016 to 2018Enrolled320ConditionsNon Ischemic Cardiomyopathy
3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 30 citations in OpenAlex.

  1. Genetic factors in the pathogenesis of cardio-oncology.Journal of translational medicine · 2024
    Review
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  7. Article
  8. Genetic polymorphisms associated with heart failure: A literature review.The Journal of international medical research · 2016
    Review
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  10. Article
  11. Review
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

11 authors at 2 institutions in 1 country.

Volker RuppertDepartment of Cardiology, University of Marburg, Germany.
Thomas Meyer
Clarissa Struwe
Jana Petersen
Andreas Perrot
Maximilian G Posch
Cemil Ozcelik
Anette Richter
Bernhard Maisch
Sabine Pankuweit
German Heart Failure Network
Philipps University of Marburg · DEMax Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cytotoxic T-lymphocyte antigen 4 (CTLA4) is an inhibitory receptor expressed on activated T cells with downregulatory properties. The aim of this study was to analyse whether single-nucleotide polymorphisms (SNPs) within the CTLA4 gene are associated with the diagnosis and disease course of dilated cardiomyopathy (DCM). In two independent cohorts of DCM patients (n=251 and 223) and healthy controls (n=591), the promoter and all four exons of the CTLA4 gene, including their flanking regions, were genotyped, and the resulting allele and genotype distributions of the identified SNPs were compared between the groups. We confirmed two known SNPs in the promoter region (-318C>T) and in exon 1 (+49A>G;Thr17Ala). The allelic frequencies and genotypic distribution of the promoter SNP were similar for DCM patients compared with controls. However, the G/G genotype of the Thr17Ala variant was significantly more frequent in DCM patients compared with controls (37 out of 251 patients (14.7%) versus 44 out of 591 controls (7.4%), P=0.005). The higher frequency of the G/G genotype was confirmed in an additional DCM cohort (29 out of 223 patients (13.0%), P=0.039), indicating that this SNP functions as a risk factor for DCM. At follow-up after 1 year, the ejection fraction and the end-diastolic diameter of the left ventricle did not differ significantly between DCM patients carrying the G/G genotype versus other genotypes (n=199). Our data indicate that the common CTLA4 variant, Thr17Ala, confers susceptibility for DCM, but does not seem to influence the course of the disease 1 year after diagnosis.

Indexed as

Genetic Predisposition to DiseaseAdultAllelesAntigens, CDCardiomyopathy, DilatedCase-Control StudiesCohort StudiesCTLA-4 AntigenDisease ProgressionFemaleGene FrequencyGenotypeHumansMaleMiddle AgedPolymorphism, Single NucleotideAntigens, CDCTLA-4 AntigenCTLA4 protein, human

Identifiers

PMID20145677
PMCPMC2987337
OpenAlexW2006684649

What OpenQuestion holds

Textmetadata
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Registered trials

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.