Evidence map›Paper›PMID 32022950›Full record

ReviewJournal of the European Academy of Dermatology and Venereology : JEADV2020

The role of the interleukin-23/Th17 pathway in cardiometabolic comorbidity associated with psoriasis.

A Egeberg, P Gisondi, J M Carrascosa, R B Warren, U Mrowietz

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of the European Academy of Dermatology and Venereology : JEADV, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

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2 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

5 authors at 5 institutions in 5 countries.

A EgebergDepartment of Dermatology and Allergy, Gentofte Hospital, Hellerup, Denmark.ORCID https://orcid.org/0000-0001-8257-1816
P GisondiSection of Dermatology and Venereology, University of Verona, Verona, Italy.ORCID https://orcid.org/0000-0002-1777-9001
J M CarrascosaDepartment of Dermatology, University Hospital Germans Trias i Pujol, Autonomous University of Barcelona (UAB), Badalona, Spain.ORCID https://orcid.org/0000-0003-4266-0771
R B WarrenDermatology Centre, Salford Royal NHS Foundation Trust, Manchester NIHR Biomedical Research Centre, The University of Manchester, Manchester, UK.
U MrowietzPsoriasis-Center at the Department of Dermatology, University Medical Center Schleswig-Holstein, Kiel, Germany.ORCID https://orcid.org/0000-0002-9539-0712
Gentofte Hospital · DKSalford Royal NHS Foundation Trust · GBUniversitat Autònoma de Barcelona · ESUniversity Hospital Schleswig-Holstein · DEUniversity of Verona · IT

Funding

Almirall R&D, Barcelona, Spain
6 · The paper itself

Abstract

Alterations in the innate and adaptive immunity underpin psoriasis pathophysiology, with the Th17 cells subset now recognized as the fundamental cells in the key controlling pathway involved in its pathogenesis. Since psoriasis is a systemic disease with important comorbidity, further knowledge on the interleukin (IL)-23/Th17 axis led to the hypothesis that there may be shared pathogenic pathways between primary skin disease and comorbidity. Psoriasis has been identified as a risk factor for cardiovascular and metabolic disease, and increasing evidence gives support to this epidemiological observation from the clinical-pathologically field. As an example, increased levels of IL-23 and IL-23R have been found in human atherosclerotic plaque, and levels correlated with symptom duration and mortality. Also, upregulation of IL-23/IL-17 seems to play an important role in both myocardial damage and stroke, with interesting reports on deleterious effect neutralization after administration of related anti-bodies in both associated conditions. In diabetic patients, increased levels of IL-23/IL-17 have also been observed and available data support a synergistic role of IL-23/IL-17 in β-cells damage. In obesity, signs of an expansion of Th17 subset in adipose tissue have been reported, as well as elevated concentrations of IL-23 in obese patients. In non-alcoholic fatty liver disease, closely related to metabolic syndrome, but also in other mentioned cardiometabolic disorders, a predominance of IL-23 and other related pro-inflammatory factors has been identified as participating in their pathogenesis. Thus, the involvement of the IL-23/Th17 axis in these shared psoriasis-cardiometabolic pathogenic mechanisms is reviewed and discussed in the light of the existing preclinical and clinical evidence, including that from comorbid psoriasis patients.

Indexed as

Cardiovascular DiseasesInterleukin-23Metabolic DiseasesPsoriasisTh17 CellsComorbidityHumansInterleukin-23

Identifiers

PMID32022950
PMCPMC7496750
OpenAlexW3004915381

What OpenQuestion holds

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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.