Evidence map›Paper›PMID 34884808›Full record

ReviewInternational journal of molecular sciences2021

Genetic Variants of the NF-κB Pathway: Unraveling the Genetic Architecture of Psoriatic Disease.

Rubén Queiro, Pablo Coto, Leire González-Lara, Eliecer Coto

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Intervention and mechanism of Xiaoyin Anshen Yin in treatment of psoriasis combined with sleep disorders.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Genetics and Epigenetics in Complex Diseases.International journal of molecular sciences · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Article
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 3 institutions in 2 countries.

Rubén QueiroRheumatology & ISPA Translational Immunology Division, Hospital Universitario Central de Asturias, 33011 Oviedo, Spain.ORCID 0000-0002-8418-7145
Pablo CotoDermatology Division, Hospital Vital Alvarez Buylla, 33611 Mieres, Spain.
Leire González-LaraDermatology Division, Hôpital Ambroise-Paré, 92100 Boulogne-Billancourt, France.
Eliecer CotoDepartment of Medicine, Oviedo University School of Medicine, 33011 Oviedo, Spain.
Universidad de Oviedo · ESFundación Renal Española · ESHôpital Ambroise-Paré · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a multifactorial genetic disease for which the genetic factors explain about 70% of disease susceptibility. Up to 30-40% of psoriasis patients develop psoriatic arthritis (PsA). However, PsA can be considered as a "disease within a disease", since in most cases psoriasis is already present when joint complaints begin. This has made studies that attempt to unravel the genetic basis for both components of psoriatic disease enormously difficult. Psoriatic disease is also accompanied by a high burden of comorbid conditions, mainly of the cardiometabolic type. It is currently unclear whether these comorbidities and psoriatic disease have a shared genetic basis or not. The nuclear factor of kappa light chain enhancer of activated B cells (NF-κB) is a transcription factor that regulates a plethora of genes in response to infection, inflammation, and a wide variety of stimuli on several cell types. This mini-review is focused on recent findings that highlight the importance of this pathway both in the susceptibility and in the determinism of some features of psoriatic disease. We also briefly review the importance of genetic variants of this pathway as biomarkers of pharmacological response. All the above may help to better understand the etiopathogenesis of this complex entity.

Indexed as

Adaptor Proteins, Signal TransducingArthritis, PsoriaticB-LymphocytesCARD Signaling Adaptor ProteinsComorbidityGenetic Predisposition to DiseaseGuanylate CyclaseHumansMembrane ProteinsNF-kappa BNF-KappaB Inhibitor alphaNF-kappa B p50 SubunitReceptors, Tumor Necrosis Factor, Type IITranscription Factor RelATumor Necrosis Factor-alphaAdaptor Proteins, Signal TransducingCARD14 protein, humanCARD Signaling Adaptor ProteinsGuanylate CyclaseMembrane ProteinsNF-kappa BNF-KappaB Inhibitor alphaNF-kappa B p50 SubunitNFKB1 protein, humanNFKBIA protein, humanNFKBIZ protein, humanReceptors, Tumor Necrosis Factor, Type IIRELA protein, humanTNF protein, humanTNFRSF1B protein, humanTranscription Factor RelATumor Necrosis Factor-alphacomorbiditiesgenetic architectureNF-κBpsoriasispsoriatic arthritis

Identifiers

PMID34884808
PMCPMC8657577
OpenAlexW3215971232

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.