Evidence map›Paper›PMID 29186830›Full record

ReviewInternational journal of molecular sciences2017

The Genetic Basis of Psoriasis.

Francesca Capon

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 8 pooled it
6.1field-weighted citation impact, top 3% 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

110 citing papers in PubMed, 8 syntheses or guidelines pooled it, 219 citations in OpenAlex.

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50 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Francesca CaponDepartment of Medical and Molecular Genetics, School of Basic and Biomedical Sciences, King's College London, London SE1 9RT, UK. francesca.capon@kcl.ac.uk.
King's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is widely regarded as a multifactorial condition which is caused by the interaction between inherited susceptibility alleles and environmental triggers. In the last decade, technological advances have enabled substantial progress in the understanding of disease genetics. Genome-wide association studies have identified more than 60 disease susceptibility regions, highlighting the pathogenic involvement of genes related to Th17 cell activation. This pathway has now been targeted by a new generation of biologics that have shown great efficacy in clinical trials. At the same time, the study of rare variants of psoriasis has identified interleukin (IL)-36 cytokines as important amplifiers of Th17 signaling and promising targets for therapeutic intervention. Here, we review these exciting discoveries, which highlight the translational potential of genetic studies.

Indexed as

Genetic Predisposition to DiseaseAnimalsCARD Signaling Adaptor ProteinsGuanylate CyclaseHumansMembrane ProteinsPolymorphism, GeneticProteinsPsoriasisCARD14 protein, humanCARD Signaling Adaptor ProteinsGuanylate CyclaseMembrane ProteinsProteinsgenome-wide association studiesgenome-wide association studies, GWASIL-36psoriasisTh17 activation

Identifiers

PMID29186830
PMCPMC5751129
OpenAlexW2768817116

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.