Evidence map›Paper›PMID 26206140›Full record

ReviewPflugers Archiv : European journal of physiology2016

Oxygen sensing in intestinal mucosal inflammation.

Katharina Flück, Joachim Fandrey

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. International journal of molecular sciences · 2022
    Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Temporal induction of intestinal epithelial hypoxia-inducible factor-2α is sufficient to drive colitis.American journal of physiology. Gastrointestinal and liver physiology · 2019
    Article
  12. Article
  13. Article
  14. Hypoxia-induced transcription factor signaling is essential for larval growth of the mosquitoProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  15. Article
  16. Article
  17. Bacteria-mediated hypoxia functions as a signal for mosquito development.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  18. Review
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.

Katharina FlückInstitut für Physiologie, Universität Duisburg-Essen, Essen, Germany.
Joachim FandreyInstitut für Physiologie, Universität Duisburg-Essen, Essen, Germany. joachim.fandrey@uni-due.de.
University of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia is a hallmark of chronically inflamed tissue. Hypoxia develops from vascular dysfunction and increased oxygen consumption by infiltrating leukocytes. With respect to inflammatory bowel disease (IBD), hypoxia is likely to be of particular importance: Impairment of the intestinal barrier during IBD allows anoxia from the lumen of the gut to spread to formerly normoxic tissue. In addition, disturbed perfusion of inflamed tissue and a higher oxygen demand of infiltrating immune cells lead to low oxygen levels in inflamed mucosal tissue. Here, cells become hypoxic and must now adapt to this condition. The hypoxia inducible factor (HIF)-1 complex is a key transcription factor for cellular adaption to low oxygen tension. HIF-1 is a heterodimer formed by two subunits: HIF-α (either HIF-1α or HIF-2α) and HIF-1β. Under normoxic conditions, hydroxylation of the HIF-α subunit by specific oxygen-dependent prolyl hydroxylases (PHDs) leads to ubiquitin proteasome-dependent degradation. Under hypoxic conditions, however, PHD activity is inhibited; thus, HIF-α can translocate into the nucleus, dimerize with HIF-1β, and bind to hypoxia-responsive elements of HIF-1 target genes. So far, most studies have addressed the function of HIF-1α in intestinal epithelial cells and the effect of HIF stabilization by PHD inhibitors in murine models of colitis. Furthermore, the role of HIF-1α in immune cells becomes more and more important as T cells or dendritic cells for which HIF-1 is of critical importance are highly involved in the pathogenesis of IBD. This review will summarize the function of HIF-1α and the therapeutic prospects for targeting the HIF pathway in intestinal mucosal inflammation.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1HumansHypoxia-Inducible Factor 1Hypoxia-Inducible Factor-Proline DioxygenasesInflammatory Bowel DiseasesIntestinal MucosaOxygenProteasome Endopeptidase ComplexBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Hypoxia-Inducible Factor 1Hypoxia-Inducible Factor-Proline DioxygenasesOxygenProteasome Endopeptidase ComplexColitisHIF-1αHydroxylaseHypoxiaImmune cellsInflammatory bowel disease

Identifiers

PMID26206140
OpenAlexW1431827665

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.