Evidence map›Paper›PMID 27713427›Full record

ArticleNature communications2016

Insulin and TOR signal in parallel through FOXO and S6K to promote epithelial wound healing.

Parisa Kakanj, Bernard Moussian, Sebastian Grönke, Victor Bustos, Sabine A Eming, Linda Partridge, Maria Leptin

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 95 citations in OpenAlex.

  1. Insulin Topical Application for Wound Healing in Nondiabetic Patients.Computational and mathematical methods in medicine · 2021
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  14. International journal of molecular sciences · 2022
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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

7 authors at 4 institutions in 3 countries.

Parisa KakanjInstitute for Genetics, University of Cologne, Zülpicherstr. 47a, Cologne 50674, Germany.
Bernard MoussianInstitute of Biology Valrose (IBV), University of Nice-Sophia Antipolis, Nice Cedex 2 06108, France.
Sebastian GrönkeMax Planck Institute for Biology of Ageing, Joseph-Stelzmann-Str. 9b, Cologne 50931, Germany.
Victor BustosMax Planck Institute for Biology of Ageing, Joseph-Stelzmann-Str. 9b, Cologne 50931, Germany.
Sabine A EmingCenter for Molecular Medicine Cologne, University of Cologne, Robert-Koch-Str. 21, Cologne 50931, Germany.
Linda PartridgeMax Planck Institute for Biology of Ageing, Joseph-Stelzmann-Str. 9b, Cologne 50931, Germany.
Maria LeptinInstitute for Genetics, University of Cologne, Zülpicherstr. 47a, Cologne 50674, Germany.ORCID http://orcid.org/0000-0001-7097-348X
University of Cologne · DEMax Planck Institute for Biology of Ageing · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversité Côte d'Azur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The TOR and Insulin/IGF signalling (IIS) network controls growth, metabolism and ageing. Although reducing TOR or insulin signalling can be beneficial for ageing, it can be detrimental for wound healing, but the reasons for this difference are unknown. Here we show that IIS is activated in the cells surrounding an epidermal wound in Drosophila melanogaster larvae, resulting in PI3K activation and redistribution of the transcription factor FOXO. Insulin and TOR signalling are independently necessary for normal wound healing, with FOXO and S6K as their respective effectors. IIS is specifically required in cells surrounding the wound, and the effect is independent of glycogen metabolism. Insulin signalling is needed for the efficient assembly of an actomyosin cable around the wound, and constitutively active myosin II regulatory light chain suppresses the effects of reduced IIS. These findings may have implications for the role of insulin signalling and FOXO activation in diabetic wound healing.

Indexed as

ActomyosinAnimalsDrosophila melanogasterDrosophila ProteinsEnzyme ActivationForkhead Transcription FactorsGene Expression RegulationGlycogenInsulinInsulin-Like Growth Factor IMyosin Type IIPhosphatidylinositol 3-KinasesRibosomal Protein S6 Kinases, 70-kDaSignal TransductionTOR Serine-Threonine KinasesWound HealingActomyosinDrosophila ProteinsForkhead Transcription FactorsFOXO protein, DrosophilaGlycogenInsulinInsulin-Like Growth Factor IMyosin Type IIPhosphatidylinositol 3-Kinasesribosomal protein S6 kinase, 70kD, polypeptide 2Ribosomal Protein S6 Kinases, 70-kDatarget of rapamycin protein, DrosophilaTOR Serine-Threonine Kinases

Identifiers

PMID27713427
PMCPMC5059774
OpenAlexW2528857537

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.