Evidence map›Paper›PMID 23798557›Full record

ArticleMolecular and cellular biology2013

Loss of epithelial hypoxia-inducible factor prolyl hydroxylase 2 accelerates skin wound healing in mice.

Joanna Kalucka, Andreas Ettinger, Kristin Franke, Soulafa Mamlouk, Rashim Pal Singh, Katja Farhat, Antje Muschter, Susanne Olbrich, Georg Breier, Dörthe M Katschinski and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2013. 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
3.0field-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

29 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. PHD1-3 oxygen sensors in vivo-lessons learned from gene deletions.Pflugers Archiv : European journal of physiology · 2024
    Review
  4. Review
  5. Article
  6. Hypoxia in Skin Cancer: Molecular Basis and Clinical Implications.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Article
  9. Impairment of the Hif-1α regulatory pathway in Foxn1-deficient (Foxn1FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
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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

13 authors at 4 institutions in 1 country.

Joanna KaluckaEmmy Noether Research Group, University of Technology, Dresden, Germany.
Andreas Ettinger
Kristin Franke
Soulafa Mamlouk
Rashim Pal Singh
Katja Farhat
Antje Muschter
Susanne Olbrich
Georg Breier
Dörthe M Katschinski
Wieland Huttner
Alexander Weidemann
Ben Wielockx
TU Dresden · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEMax Planck Institute of Molecular Cell Biology and Genetics · DEUniversitätsmedizin Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skin wound healing in mammals is a complex, multicellular process that depends on the precise supply of oxygen. Hypoxia-inducible factor (HIF) prolyl hydroxylase 2 (PHD2) serves as a crucial oxygen sensor and may therefore play an important role during reepithelialization. Hence, this study was aimed at understanding the role of PHD2 in cutaneous wound healing using different lines of conditionally deficient mice specifically lacking PHD2 in inflammatory, vascular, or epidermal cells. Interestingly, PHD2 deficiency only in keratinocytes and not in myeloid or endothelial cells was found to lead to faster wound closure, which involved enhanced migration of the hyperproliferating epithelium. We demonstrate that this effect relies on the unique expression of β3-integrin in the keratinocytes around the tip of the migrating tongue in an HIF1α-dependent manner. Furthermore, we show enhanced proliferation of these cells in the stratum basale, which is directly related to their attenuated transforming growth factor β signaling. Thus, loss of the central oxygen sensor PHD2 in keratinocytes stimulates wound closure by prompting skin epithelial cells to migrate and proliferate. Inhibition of PHD2 could therefore offer novel therapeutic opportunities for the local treatment of cutaneous wounds.

Indexed as

Gene Knockout TechniquesWound HealingAnimalsCell MovementCell ProliferationGene Expression RegulationHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesIntegrin beta3KeratinocytesMaleMiceMice, KnockoutProcollagen-Proline DioxygenaseSkinSkin Physiological PhenomenaEgln1 protein, mouseHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesIntegrin beta3Procollagen-Proline DioxygenaseTransforming Growth Factor beta

Identifiers

PMID23798557
PMCPMC3753847
OpenAlexW2163348987

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.