Evidence map›Paper›PMID 25569246›Full record

ArticlePloS one2015

Gene therapy of c-myc suppressor FUSE-binding protein-interacting repressor by Sendai virus delivery prevents tracheal stenosis.

Daisuke Mizokami, Koji Araki, Nobuaki Tanaka, Hiroshi Suzuki, Masayuki Tomifuji, Taku Yamashita, Yasuji Ueda, Hideaki Shimada, Kazuyuki Matsushita, Akihiro Shiotani

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
    Review
  2. Preclinical Vocal Fold and Airway Injury Models: A Scoping Review.Laryngoscope investigative otolaryngology · 2025
    Review
  3. Review
  4. Article
  5. 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

10 authors at 4 institutions in 1 country.

Daisuke MizokamiDepartment of Otolaryngology, Head & Neck Surgery, National Defense Medical College, Tokorozawa, Saitama, Japan.
Koji ArakiDepartment of Otolaryngology, Head & Neck Surgery, National Defense Medical College, Tokorozawa, Saitama, Japan.
Nobuaki TanakaDepartment of Otolaryngology, Head & Neck Surgery, National Defense Medical College, Tokorozawa, Saitama, Japan.
Hiroshi SuzukiDepartment of Otolaryngology, Head & Neck Surgery, National Defense Medical College, Tokorozawa, Saitama, Japan.
Masayuki TomifujiDepartment of Otolaryngology, Head & Neck Surgery, National Defense Medical College, Tokorozawa, Saitama, Japan.
Taku YamashitaDepartment of Otolaryngology, Head & Neck Surgery, National Defense Medical College, Tokorozawa, Saitama, Japan.
Yasuji UedaDNAVEC Corporation, Tsukuba, Ibaraki, Japan.
Hideaki ShimadaDepartment of Surgery, Toho University School of Medicine, Ota-Ku, Tokyo, Japan.
Kazuyuki MatsushitaDepartment of Molecular Diagnosis (F8), Chiba University Graduate School of Medicine, Chiba City, Chiba, Japan.
Akihiro ShiotaniDepartment of Otolaryngology, Head & Neck Surgery, National Defense Medical College, Tokorozawa, Saitama, Japan.
National Defense Medical College · JPChiba University · JPID Pharma (Japan) · JPToho University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acquired tracheal stenosis remains a challenging problem for otolaryngologists. The objective of this study was to determine whether the Sendai virus (SeV)-mediated c-myc suppressor, a far upstream element (FUSE)-binding protein (FBP)-interacting repressor (FIR), modulates wound healing of the airway mucosa, and whether it prevents tracheal stenosis in an animal model of induced mucosal injury. A fusion gene-deleted, non-transmissible SeV vector encoding FIR (FIR-SeV/ΔF) was prepared. Rats with scraped airway mucosae were administered FIR-SeV/ΔF through the tracheostoma. The pathological changes in the airway mucosa and in the tracheal lumen were assessed five days after scraping. Untreated animals showed hyperplasia of the airway epithelium and a thickened submucosal layer with extensive fibrosis, angiogenesis, and collagen deposition causing lumen stenosis. By contrast, the administration of FIR-SeV/ΔF decreased the degree of tracheal stenosis (P < 0.05) and improved the survival rate (P < 0.05). Immunohistochemical staining showed that c-Myc expression was downregulated in the tracheal basal cells of the FIR-SeV/ΔF-treated animals, suggesting that c-myc was suppressed by FIR-SeV/ΔF in the regenerating airway epithelium of the injured tracheal mucosa. The airway-targeted gene therapy of the c-myc suppressor FIR, using a recombinant SeV vector, prevented tracheal stenosis in a rat model of airway mucosal injury.

Indexed as

AnimalsDisease Models, AnimalFemaleGenetic TherapyGenetic VectorsImmunohistochemistryKaplan-Meier EstimateProto-Oncogene Proteins c-mycRatsRats, Sprague-DawleyRepressor ProteinsRNA-Binding ProteinsRNA Splicing FactorsSendai virusTracheaTracheal Stenosispoly-U binding splicing factor 60KDaProto-Oncogene Proteins c-mycRepressor ProteinsRNA-Binding ProteinsRNA Splicing Factors

Identifiers

PMID25569246
PMCPMC4287628
OpenAlexW2072326765

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.