Evidence map›Paper›PMID 29073253›Full record

ArticlePloS one2017

Nrf2 is highly expressed in neutrophils, but myeloid cell-derived Nrf2 is dispensable for wound healing in mice.

Natasha Joshi, Sabine Werner

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Redox regulation of the immune response.Cellular & molecular immunology · 2022
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Macrophage mediation in normal and diabetic wound healing responses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. 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.

Natasha JoshiDepartment of Biology, Institute of Molecular Health Sciences, Swiss Federal Institute of Technology (ETH) Zurich, Otto-Stern-Weg 7, Zurich, Switzerland.
Sabine WernerDepartment of Biology, Institute of Molecular Health Sciences, Swiss Federal Institute of Technology (ETH) Zurich, Otto-Stern-Weg 7, Zurich, Switzerland.ORCID http://orcid.org/0000-0001-7397-8710
ETH Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune cells of the myeloid lineage are key players in skin wound healing, since they secrete various cytokines and growth factors that orchestrate the repair process. In addition, they are crucial for the defense against invading pathogens through their capacity to produce high levels of reactive oxygen species (ROS). To limit the toxicity of ROS, cells have developed antioxidant defense strategies, including expression of the cytoprotective NRF2 transcription factor. Here we show that murine neutrophils and to a lesser extent macrophages strongly express Nrf2 already when present in the circulation and in particular at the wound site. To determine the role of Nrf2 in neutrophils and macrophages for wound repair, we generated mice with a gain- or loss-of-function of this transcription factor in the myeloid cell lineage. Expression of a constitutively active Nrf2 mutant in myeloid cells did not further enhance the overall Nrf2 activity in these cells due to the already high steady-state activity of endogenous Nrf2. Surprisingly, deletion of Nrf2 in myeloid cells only mildly affected the levels of ROS and the expression of pro-inflammatory cytokines by these cells. In particular, various parameters of wound healing, including wound closure, reepithelialization, wound contraction and the presence of myeloid cells at the wound site were not affected. These results reveal that Nrf2 in myeloid cells is dispensable for wound healing and suggest the presence of additional antioxidant defense strategies of these cells that compensate for the loss of Nrf2, even in the harsh environment of skin wounds.

Indexed as

Wound HealingAnimalsFlow CytometryMiceNeutrophilsNF-E2-Related Factor 2Reverse Transcriptase Polymerase Chain ReactionSkinNfe2l2 protein, mouseNF-E2-Related Factor 2

Identifiers

PMID29073253
PMCPMC5658185
OpenAlexW2765899666

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.