Evidence map›Paper›PMID 25045210›Full record

ReviewMediators of inflammation2014

Tumour necrosis factor superfamily members in the pathogenesis of inflammatory bowel disease.

Tomasz J Ślebioda, Zbigniew Kmieć

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04733456 (Evaluation of Brain Activity and Oxygenation Using Near-infrared Spectroscopy), which is not on this map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
8.6field-weighted citation impact, top 2% 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.

NCT04733456 unknown statusnot on this mapstarted 2021, after this paper: background citation

Evaluation of Brain Activity and Oxygenation Using Near-infrared Spectroscopy (NIRS) in Inflammatory Bowel Disease (IBD) Patients

TypeobservationalSponsorUniversity of CalgaryRan2021 to 2026Enrolled40ConditionsIBD, Maladaptive Behavior Associated With Physical IllnessArmsQuality of life questionnaires, NIRS, Stool Collection, Blood and urine collection
3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 100 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. The Impact of Genetic Variation on Drug Response in Adult IBD: A Systematic Review.JGH open : an open access journal of gastroenterology and hepatology · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. The Antioxidant Properties ofAntioxidants (Basel, Switzerland) · 2023
    Article
  11. Review
  12. Review
  13. Gastrointestinal Changes and Alzheimer's Disease.Current Alzheimer research · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Standardized Fraction ofBiomolecules · 2020
    Article
  18. The role of FAS gene variants in inflammatory bowel disease.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2020
    Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Tomasz J ŚlebiodaDepartment of Histology, Medical University of Gdańsk, Dębinki 1, 80-211 Gdańsk, Poland.
Zbigniew KmiećDepartment of Histology, Medical University of Gdańsk, Dębinki 1, 80-211 Gdańsk, Poland.
Gdańsk Medical University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a group of inflammatory conditions of the gastrointestinal tract of unclear aetiology of which two major forms are Crohn's disease (CD) and ulcerative colitis (UC). CD and UC are immunologically distinct, although they both result from hyperactivation of proinflammatory pathways in intestines and disruption of intestinal epithelial barrier. Members of the tumour necrosis factor superfamily (TNFSF) are molecules of broad spectrum of activity, including direct disruption of intestinal epithelial barrier integrity and costimulation of proinflammatory functions of lymphocytes. Tumour necrosis factor (TNF) has a well-established pathological role in IBD which also serves as a target in IBD treatment. In this review we discuss the role of TNF and other TNFSF members, notably, TL1A, FasL, LIGHT, TRAIL, and TWEAK, in the pathogenesis of IBD.

Indexed as

AnimalsCytokine TWEAKFas Ligand ProteinHumansInflammatory Bowel DiseasesTNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor-alphaTumor Necrosis Factor Ligand Superfamily Member 14Tumor Necrosis Factor Ligand Superfamily Member 15Tumor Necrosis FactorsCytokine TWEAKFas Ligand ProteinTNF-Related Apoptosis-Inducing LigandTNFSF12 protein, humanTNFSF15 protein, humanTumor Necrosis Factor-alphaTumor Necrosis Factor Ligand Superfamily Member 14Tumor Necrosis Factor Ligand Superfamily Member 15Tumor Necrosis Factors

Identifiers

PMID25045210
PMCPMC4087264
OpenAlexW2061625478

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.