Evidence map›Paper›PMID 31668626›Full record

ArticleCurrent biology : CB2019

Injury Activates a Dynamic Cytoprotective Network to Confer Stress Resilience and Drive Repair.

Helen Weavers, Will Wood, Paul Martin

Open access · hybridAbstract read
In one paragraph

Article in Current biology : CB, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Cellular and molecular mechanisms of skin wound healing.Nature reviews. Molecular cell biology · 2024
    Review
  10. Biological resilience in health and disease.Disease models & mechanisms · 2024
    Review
  11. Article
  12. Macrophage Nrf 2 the rescue.The Journal of cell biology · 2023
    Article
  13. Article
  14. Targeting NRF2 to promote epithelial repair.Biochemical Society transactions · 2023
    Review
  15. Parallel repair mechanisms in plants and animals.Disease models & mechanisms · 2023
    Article
  16. Article
  17. Wound Healing Insights from Flies and Fish.Cold Spring Harbor perspectives in biology · 2022
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Helen WeaversSchool of Biochemistry, Biomedical Sciences, University of Bristol, Bristol BS8 1TD, UK. Electronic address: helen.weavers@bristol.ac.uk.
Will WoodSchool of Cellular and Molecular Medicine, Biomedical Sciences, University of Bristol, Bristol BS8 1TD, UK; Centre for Inflammation Research, University of Edinburgh, Queens Medical Research Institute, Edinburgh EH16 4TJ, UK.
Paul MartinSchool of Biochemistry, Biomedical Sciences, University of Bristol, Bristol BS8 1TD, UK; School of Physiology, Pharmacology and Neuroscience, Biomedical Sciences, University of Bristol, Bristol BS8 1TD, UK; School of Medicine, Cardiff University, Cardiff CF14 4XN, UK.
University of Bristol · GB

Funding

Medical Research Council MR/J002577/1Wellcome Trust 208762/Z/17/Z
6 · The paper itself

Abstract

In healthy individuals, injured tissues rapidly repair themselves following damage. Within a healing skin wound, recruited inflammatory cells release a multitude of bacteriocidal factors, including reactive oxygen species (ROS), to eliminate invading pathogens. Paradoxically, while these highly reactive ROS confer resistance to infection, they are also toxic to host tissues and may ultimately delay repair. Repairing tissues have therefore evolved powerful cytoprotective "resilience" machinery to protect against and tolerate this collateral damage. Here, we use in vivo time-lapse imaging and genetic manipulation in Drosophila to dissect the molecular and cellular mechanisms that drive tissue resilience to wound-induced stress. We identify a dynamic, cross-regulatory network of stress-activated cytoprotective pathways, linking calcium, JNK, Nrf2, and Gadd45, that act to both "shield" tissues from oxidative damage and promote efficient damage repair. Ectopic activation of these pathways confers stress protection to naive tissue, while their inhibition leads to marked delays in wound closure. Strikingly, the induction of cytoprotection is tightly linked to the pathways that initiate the inflammatory response, suggesting evolution of a fail-safe mechanism for tissue protection each time inflammation is triggered. A better understanding of these resilience mechanisms-their identities and precise spatiotemporal regulation-is of major clinical importance for development of therapeutic interventions for all pathologies linked to oxidative stress, including debilitating chronic non-healing wounds.

Indexed as

AnimalsCalciumCytoprotectionDrosophila melanogasterDrosophila ProteinsGADD45 ProteinsInflammationIntracellular Signaling Peptides and ProteinsMAP Kinase Signaling SystemNF-E2-Related Factor 2Oxidation-ReductionOxidative StressReactive Oxygen SpeciesWound HealingCalciumDrosophila ProteinsGADD45 ProteinsIntracellular Signaling Peptides and ProteinsNF-E2-Related Factor 2Reactive Oxygen SpeciescytoprotectionDNA damagehormesisinflammationoxidative stresspreconditioningROStissue repairtissue resiliencewound

Identifiers

PMID31668626
PMCPMC6868510
OpenAlexW2981933359

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.