Evidence map›Paper›PMID 25477373›Full record

ReviewAmerican journal of physiology. Gastrointestinal and liver physiology2015

Redeeming an old foe: protective as well as pathophysiological roles for tumor necrosis factor in inflammatory bowel disease.

Philip E Dubé, Shivesh Punit, D Brent Polk

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Gastrointestinal and liver physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Proton FLASH Exposure Preserves Gut Commensal Microbiomes and Spares Intestinal Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
  4. Review
  5. Role of Sam68 as an adaptor protein in inflammatory signaling.Cellular and molecular life sciences : CMLS · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Targeting tumor necrosis factor receptors in ankylosing spondylitis.Annals of the New York Academy of Sciences · 2019
    Review
  15. Article
  16. Article
  17. Activation of TGF-Physiological reports · 2017
    Article
  18. Review
  19. Article
  20. Induction of Colonic M Cells during Intestinal Inflammation.The American journal of pathology · 2016
    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

3 authors at 2 institutions in 1 country.

Philip E DubéSaban Research Institute, Children's Hospital Los Angeles, Los Angeles, California; Department of Pediatrics, Children's Hospital Los Angeles and University of Southern California Keck School of Medicine, Los Angeles, California; and.
Shivesh PunitSaban Research Institute, Children's Hospital Los Angeles, Los Angeles, California; Department of Pediatrics, Children's Hospital Los Angeles and University of Southern California Keck School of Medicine, Los Angeles, California; and.
D Brent PolkSaban Research Institute, Children's Hospital Los Angeles, Los Angeles, California; Department of Pediatrics, Children's Hospital Los Angeles and University of Southern California Keck School of Medicine, Los Angeles, California; and Department of Biochemistry and Molecular Biology, University of Southern California Keck School of Medicine, Los Angeles, California dbpolk@chla.usc.edu.
University of Southern California · USChildren's Hospital of Los Angeles · US

Funding

CYTOKINE REGULATION OF INTESTINAL EPITHELIAL RESTITUTIONR01DK056008 · NIDDK · VANDERBILT UNIVERSITY · PI POLK, D BRENT · 1999 to 2020
$6.8M
Mechanisms of KSR regulation in intestinal cell survivalR01DK066176 · NIDDK · VANDERBILT UNIVERSITY · PI POLK, D BRENT · 2005 to 2009
$1.7M
REGULATION OF INTESTINAL EPITHELIAL CELL MIGRATIONR01DK054993 · NIDDK · VANDERBILT UNIVERSITY · PI POLK, D. BRENT · 2001 to 2005
$1.1M
Canadian Institutes of Health ResearchNIDDK NIH HHS R01 DK-056008NIDDK NIH HHS R01 DK056008NIDDK NIH HHS R01 DK-066176NIDDK NIH HHS R01 DK-54993
6 · The paper itself

Abstract

Tumor necrosis factor (TNF) and its receptors TNFR1 and TNFR2 are major therapeutic targets for inflammatory bowel disease. Research advances have demonstrated that TNF produces pleiotropic responses in the gastrointestinal (GI) tract. Although in excess TNF can contribute to GI pathology, TNF is also a critical protective factor to promote GI homeostasis following injury and inflammation. Genetic studies using candidate and genome-wide association study approaches have identified variants in TNF or its receptors that are associated with Crohn's disease or ulcerative colitis in multiple populations, although the basis for these associations remains unclear. This review considers the efficacy and mechanism of anti-TNF therapies for inflammatory bowel disease to reconcile the many disparate aspects of TNF research and to consider the potential protective effects of TNF signaling in GI health.

Indexed as

AnimalsAntibodies, MonoclonalGastrointestinal AgentsGastrointestinal TractHumansInflammatory Bowel DiseasesReceptors, Tumor Necrosis FactorTumor Necrosis FactorsAntibodies, MonoclonalGastrointestinal AgentsReceptors, Tumor Necrosis FactorTumor Necrosis Factorsinflammatory bowel diseasetumor necrosis factortumor necrosis factor receptor 1tumor necrosis factor receptor 2

Identifiers

PMID25477373
PMCPMC4312954
OpenAlexW2112198303

What OpenQuestion holds

Textmetadata
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.