Evidence map›Paper›PMID 25010393›Full record

ArticleThe American journal of pathology2014

Reduced FOXO1 expression accelerates skin wound healing and attenuates scarring.

Ryoichi Mori, Katsuya Tanaka, Maiko de Kerckhove, Momoko Okamoto, Kazuya Kashiyama, Katsumi Tanaka, Sangeun Kim, Takuya Kawata, Toshimitsu Komatsu, Seongjoon Park and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  5. Hypoxia reveals a new function of Foxn1 in the keratinocyte antioxidant defense system.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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  13. Characterization of Burn Eschar Pericytes.Journal of clinical medicine · 2020
    Article
  14. Article
  15. Transcriptomic Analysis of Cellular Pathways in Healing Flexor Tendons of Plasminogen Activator Inhibitor 1 (PAI-1/Serpine1) Null Mice.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020
    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

14 authors at 3 institutions in 2 countries.

Ryoichi MoriDepartment of Pathology, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Electronic address: ryoichi@nagasaki-u.ac.jp.
Katsuya TanakaDepartment of Pathology, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan; Department of Plastic and Reconstructive Surgery, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Maiko de KerckhoveDepartment of Pathology, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan; Center for Medical Education and Research, Nagasaki Municipal Hospital, Nagasaki, Japan.
Momoko OkamotoDepartment of Pathology, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Kazuya KashiyamaDepartment of Plastic and Reconstructive Surgery, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Katsumi TanakaDepartment of Plastic and Reconstructive Surgery, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Sangeun KimDepartment of Pathology, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Takuya KawataDepartment of Pathology, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Toshimitsu KomatsuDepartment of Pathology, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Seongjoon ParkDepartment of Pathology, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Kazuya IkematsuDepartment of Forensic Pathology and Science, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Akiyoshi HiranoDepartment of Plastic and Reconstructive Surgery, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Paul MartinSchools of Biochemistry and Physiology and Pharmacology, Faculty of Medical and Veterinary Sciences, University of Bristol, Bristol, United Kingdom.
Isao ShimokawaDepartment of Pathology, School of Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Nagasaki University · JPNagasaki Municipal Hospital · JPUniversity of Bristol · GB

Funding

Wellcome TrustWellcome Trust 097791MA
6 · The paper itself

Abstract

The forkhead box O (FOXO) family has been extensively investigated in aging and metabolism, but its role in tissue-repair processes remains largely unknown. Herein, we clarify the molecular aspect of the FOXO family in skin wound healing. We demonstrated that Foxo1 and Foxo3a were both up-regulated during murine skin wound healing. Partial knockout of Foxo1 in Foxo1(+/-) mice throughout the body led to accelerated skin wound healing with enhanced keratinocyte migration, reduced granulation tissue formation, and decreased collagen density, accompanied by an attenuated inflammatory response, but we observed no wound phenotype in Foxo3a(-/-) mice. Fibroblast growth factor 2, adiponectin, and notch1 genes were significantly increased at wound sites in Foxo1(+/-) mice, along with markedly altered extracellular signal-regulated kinase 1/2 and AKT phosphorylation. Similarly, transient knockdown of Foxo1 at the wound site by local delivery of antisense oligodeoxynucleotides enhanced skin wound healing. The link between FOXO1 and scarring extends to patients, in particular keloid scars, where we see FOXO1 expression markedly increased in fibroblasts and inflammatory cells within the otherwise normal dermis. This occurs in the immediate vicinity of the keloid by comparison to the center of the mature keloid, indicating that FOXO1 is associated with the overgrowth of this fibrotic response into adjacent normal skin. Overall, our data indicate that molecular targeting of FOXO1 may improve the quality of healing and reduce pathological scarring.

Indexed as

AnimalsBlotting, WesternCicatrixDisease Models, AnimalEnzyme-Linked Immunosorbent AssayForkhead Box Protein O1Forkhead Transcription FactorsHumansKeloidMacrophagesMiceMice, KnockoutMicroscopy, Electron, TransmissionOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionWound HealingForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanFoxo1 protein, mouse

Identifiers

PMID25010393
PMCPMC4188279
OpenAlexW2164438840

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.