Evidence map›Paper›PMID 26512123›Full record

ReviewDisease models & mechanisms2015

Exploring the HIFs, buts and maybes of hypoxia signalling in disease: lessons from zebrafish models.

Philip M Elks, Stephen A Renshaw, Annemarie H Meijer, Sarah R Walmsley, Fredericus J van Eeden

Open access · goldAbstract readReview
In one paragraph

Review in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 66 citations in OpenAlex.

  1. Toxics · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Zebrafish-An Optimal Model in Experimental Oncology.Molecules (Basel, Switzerland) · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Using the Zebrafish as a Genetic Model to Study Erythropoiesis.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Deficiency in Neuroserpin Exacerbates CoClFrontiers in pharmacology · 2021
    Article
  16. Article
  17. Article
  18. 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

5 authors at 3 institutions in 2 countries.

Philip M ElksDepartment of Infection and Immunity, Medical School, The University of Sheffield, Sheffield, S10 2RX, UK The Bateson Centre, The University of Sheffield, Sheffield, S10 2TN, UK p.elks@sheffield.ac.uk.
Stephen A RenshawDepartment of Infection and Immunity, Medical School, The University of Sheffield, Sheffield, S10 2RX, UK The Bateson Centre, The University of Sheffield, Sheffield, S10 2TN, UK.
Annemarie H MeijerInstitute of Biology, Leiden University, 2333 CC Leiden, The Netherlands.
Sarah R WalmsleyMRC Centre for Inflammation Research, University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Fredericus J van EedenThe Bateson Centre, The University of Sheffield, Sheffield, S10 2TN, UK.
University of Sheffield · GBCentre for Inflammation Research · GBLeiden University · NL

Funding

Medical Research Council G0700091Medical Research Council G0701932Medical Research Council G108/595Medical Research Council MR/K006312/1Medical Research Council MR/M004864/1Wellcome Trust 098516Wellcome Trust 105570Wellcome Trust 105570/Z/14/Z
6 · The paper itself

Abstract

A low level of tissue oxygen (hypoxia) is a physiological feature of a wide range of diseases, from cancer to infection. Cellular hypoxia is sensed by oxygen-sensitive hydroxylase enzymes, which regulate the protein stability of hypoxia-inducible factor α (HIF-α) transcription factors. When stabilised, HIF-α binds with its cofactors to HIF-responsive elements (HREs) in the promoters of target genes to coordinate a wide-ranging transcriptional programme in response to the hypoxic environment. This year marks the 20th anniversary of the discovery of the HIF-1α transcription factor, and in recent years the HIF-mediated hypoxia response is being increasingly recognised as an important process in determining the outcome of diseases such as cancer, inflammatory disease and bacterial infections. Animal models have shed light on the roles of HIF in disease and have uncovered intricate control mechanisms that involve multiple cell types, observations that might have been missed in simpler in vitro systems. These findings highlight the need for new whole-organism models of disease to elucidate these complex regulatory mechanisms. In this Review, we discuss recent advances in our understanding of hypoxia and HIFs in disease that have emerged from studies of zebrafish disease models. Findings from such models identify HIF as an integral player in the disease processes. They also highlight HIF pathway components and their targets as potential therapeutic targets against conditions that range from cancers to infectious disease.

Indexed as

Cellular MicroenvironmentSignal TransductionAnimalsAryl Hydrocarbon Receptor Nuclear TranslocatorBasic Helix-Loop-Helix ProteinsCell HypoxiaDrug DesignEndothelial PAS Domain-Containing Protein 1HumansHypoxia-Inducible Factor 1, alpha SubunitModels, AnimalMolecular Targeted TherapyOxygenSpecies SpecificityTranscription FactorsZebrafisharnt protein, zebrafishAryl Hydrocarbon Receptor Nuclear TranslocatorBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Hypoxia-Inducible Factor 1, alpha SubunitOxygenTranscription FactorsZebrafish ProteinsDisease modelsHypoxiaHypoxia-inducible factorZebrafish

Identifiers

PMID26512123
PMCPMC4631790
OpenAlexW2097784885

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.