Evidence map›Paper›PMID 29339718›Full record

ArticleNature communications2018

Injury-activated glial cells promote wound healing of the adult skin in mice.

Vadims Parfejevs, Julien Debbache, Olga Shakhova, Simon M Schaefer, Mareen Glausch, Michael Wegner, Ueli Suter, Una Riekstina, Sabine Werner, Lukas Sommer

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
12.5field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 195 citations in OpenAlex.

  1. Review
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  13. Glia of the heart's nervous system.Nature reviews. Neuroscience · 2025
    Review
  14. Article
  15. Review
  16. Review
  17. Fibroblast-Mediated Macrophage Recruitment Supports Acute Wound Healing.The Journal of investigative dermatology · 2025
    Article
  18. Review
  19. Article
  20. Endometriosis and Adenomyosis: From Pathogenesis to Follow-Up.Current issues in molecular biology · 2025
    Review

36 more citing papers are in PubMed but not listed here.

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

10 authors at 5 institutions in 3 countries.

Vadims ParfejevsInstitute of Anatomy, University of Zürich, 8057, Zürich, Switzerland.
Julien DebbacheInstitute of Anatomy, University of Zürich, 8057, Zürich, Switzerland.
Olga ShakhovaDepartment of Oncology, University Hospital Zürich, 8952, Schlieren, Switzerland.
Simon M SchaeferInstitute of Anatomy, University of Zürich, 8057, Zürich, Switzerland.
Mareen GlauschInstitute of Anatomy, University of Zürich, 8057, Zürich, Switzerland.
Michael WegnerInstitute of Biochemistry, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91054, Erlangen, Germany.
Ueli SuterInstitute of Molecular Health Sciences, ETH, 8093, Zürich, Switzerland.
Una RiekstinaFaculty of Medicine, University of Latvia, Raina Blvd., LV 1586, Riga, Latvia.
Sabine WernerInstitute of Molecular Health Sciences, ETH, 8093, Zürich, Switzerland.
Lukas SommerInstitute of Anatomy, University of Zürich, 8057, Zürich, Switzerland. lukas.sommer@anatom.uzh.ch.
University of Zurich · CHETH Zurich · CHFriedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity Hospital of Zurich · CHUniversity of Latvia · LV

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cutaneous wound healing is a complex process that aims to re-establish the original structure of the skin and its functions. Among other disorders, peripheral neuropathies are known to severely impair wound healing capabilities of the skin, revealing the importance of skin innervation for proper repair. Here, we report that peripheral glia are crucially involved in this process. Using a mouse model of wound healing, combined with in vivo fate mapping, we show that injury activates peripheral glia by promoting de-differentiation, cell-cycle re-entry and dissemination of the cells into the wound bed. Moreover, injury-activated glia upregulate the expression of many secreted factors previously associated with wound healing and promote myofibroblast differentiation by paracrine modulation of TGF-β signalling. Accordingly, depletion of these cells impairs epithelial proliferation and wound closure through contraction, while their expansion promotes myofibroblast formation. Thus, injury-activated glia and/or their secretome might have therapeutic potential in human wound healing disorders.

Indexed as

AnimalsCell CycleCell DifferentiationCells, CulturedGene Expression ProfilingHumansMice, 129 StrainMice, Inbred C57BLMice, Inbred DBAMice, KnockoutMice, TransgenicMyofibroblastsNeurogliaSignal TransductionSkinSOXE Transcription FactorsSox10 protein, mouseSOXE Transcription FactorsTransforming Growth Factor beta

Identifiers

PMID29339718
PMCPMC5770460
OpenAlexW2783115864

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.