Evidence map›Paper›PMID 28232470›Full record

ArticleThe Journal of experimental medicine2017

Epithelial Fli1 deficiency drives systemic autoimmunity and fibrosis: Possible roles in scleroderma.

Takehiro Takahashi, Yoshihide Asano, Koji Sugawara, Takashi Yamashita, Kouki Nakamura, Ryosuke Saigusa, Yohei Ichimura, Tetsuo Toyama, Takashi Taniguchi, Kaname Akamata and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
8.7field-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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The mRNA levels ofPostepy dermatologii i alergologii · 2026
    Article
  4. Targeting endothelial ERG to mitigate vascular regression in retinopathies.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Pericytes mediate neuroinflammation via Fli-1 in endotoxemia and sepsis in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  6. Article
  7. Article
  8. Silencing ofJournal of the American Heart Association · 2023
    Article
  9. Current Concepts on the Pathogenesis of Systemic Sclerosis.Clinical reviews in allergy & immunology · 2023
    Review
  10. Fli1 and Tissue Fibrosis in Various Diseases.International journal of molecular sciences · 2023
    Review
  11. Contribution of keratinocytes to dermal fibrosis.Current opinion in rheumatology · 2022
    Review
  12. Article
  13. Suppression of Fli-1 protects against pericyte loss and cognitive deficits in Alzheimer's disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  14. Article
  15. Observational
  16. A Genome-wide Association Study Identifies SERPINB10, CRLF3, STX7, LAMP3, IFNG-AS1, and KRT80 As Risk Loci Contributing to Cutaneous Leishmaniasis in Brazil.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 2 countries.

Takehiro TakahashiDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.
Yoshihide AsanoDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan yasano-tky@umin.ac.jp.ORCID 0000-0001-5560-9778
Koji SugawaraDepartment of Dermatology, Osaka City University Graduate School of Medicine, Abeno-ku, Osaka 545-8585, Japan.
Takashi YamashitaDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.ORCID 0000-0002-4740-5692
Kouki NakamuraDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.
Ryosuke SaigusaDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.
Yohei IchimuraDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.
Tetsuo ToyamaDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.
Takashi TaniguchiDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.
Kaname AkamataDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.
Shinji NodaDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.
Ayumi YoshizakiDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.
Daisuke TsurutaDepartment of Dermatology, Osaka City University Graduate School of Medicine, Abeno-ku, Osaka 545-8585, Japan.
Maria TrojanowskaArthritis Center, Rheumatology, Boston University School of Medicine, Boston, MA 02118.
Shinichi SatoDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.ORCID 0000-0001-5519-172X
The University of Tokyo · JPOsaka City University · JPBoston University · US

Funding

The molecular mechanisms of fibrosisR01AR042334 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1994 to 2018
$5.2M
TGF-beta receptor/Endoglin signaling and the origin of scleroderma fibroblastR56AR044883 · NIAMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI TROJANOWSKA, MARIA · 2015 to 2015
$410k
NIAMS NIH HHS R01 AR042334NIAMS NIH HHS R56 AR044883
6 · The paper itself

Abstract

Systemic sclerosis (SSc), or scleroderma, is a multisystem autoimmune disorder characterized by vasculopathy and fibrosis in the skin and internal organs, most frequently in the esophagus and lungs. Hitherto, studies on SSc pathogenesis centered on immune cells, vascular cells, and fibroblasts. Although dysregulated keratinocytes in SSc have been recently reported, the contribution of epithelial cells to pathogenesis remains unexplored. In this study, we demonstrated the induction of SSc-like molecular phenotype in keratinocytes by gene silencing of transcription factor Friend leukemia virus integration 1 (Fli1), the deficiency of which is implicated in SSc pathogenesis. Keratin 14-expressing epithelial cell-specific

Indexed as

AutoimmunityAIRE ProteinAnimalsDisease Models, AnimalEpithelial CellsEsophagusFibrosisHomeodomain ProteinsHumansKeratin-14KeratinocytesMiceProto-Oncogene Protein c-fli-1Scleroderma, SystemicSkinTh17 CellsAIRE ProteinFLI1 protein, humanFli1 protein, mouseHomeodomain ProteinsKeratin-14Proto-Oncogene Protein c-fli-1RAG-1 proteinTranscription Factors

Identifiers

PMID28232470
PMCPMC5379967
OpenAlexW2590491928

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.