Evidence map›Paper›PMID 22433854›Full record

ArticleThe Journal of biological chemistry2012

Sensitivity of heterozygous α1,6-fucosyltransferase knock-out mice to cigarette smoke-induced emphysema: implication of aberrant transforming growth factor-β signaling and matrix metalloproteinase gene expression.

Congxiao Gao, Toshitaka Maeno, Fumi Ota, Manabu Ueno, Hiroaki Korekane, Shinji Takamatsu, Ken Shirato, Akio Matsumoto, Satoshi Kobayashi, Keiichi Yoshida and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.2field-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

28 citing papers in PubMed, 69 citations in OpenAlex.

  1. Emerging Mechanistic Links Between Fucosylation and Senescence in Lung Diseases.Journal of respiratory biology and translational medicine · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
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  10. Review
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  14. Review
  15. Article
  16. N-Glycosylation.Advances in experimental medicine and biology · 2021
    Article
  17. Review
  18. 3D Structure and Function of Glycosyltransferases Involved inInternational journal of molecular sciences · 2020
    Review
  19. Article
  20. Core-Fucosylated Tetra-AntennaryInternational journal of molecular sciences · 2019
    Article
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 5 institutions in 1 country.

Congxiao GaoRIKEN Alliance Laboratory, The Institute of Scientific and Industrial Research, Osaka University, Osaka 567-0047, Japan.
Toshitaka Maeno
Fumi Ota
Manabu Ueno
Hiroaki Korekane
Shinji Takamatsu
Ken Shirato
Akio Matsumoto
Satoshi Kobayashi
Keiichi Yoshida
Shinobu Kitazume
Kazuaki Ohtsubo
Tomoko Betsuyaku
Naoyuki Taniguchi
Osaka University · JPRIKEN Advanced Science Institute · JPGunma University · JPKeio University · JPWaseda University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously demonstrated that a deficiency in core fucosylation caused by the genetic disruption of α1,6-fucosyltransferase (Fut8) leads to lethal abnormalities and the development of emphysematous lesions in the lung by attenuation of TGF-β1 receptor signaling. Herein, we investigated the physiological relevance of core fucosylation in the pathogenesis of emphysema using viable heterozygous knock-out mice (Fut8(+/-)) that were exposed to cigarette smoke (CS). The Fut8(+/-) mice exhibited a marked decrease in FUT8 activity, and matrix metalloproteinase (MMP)-9 activities were elevated in the lung at an early stage of exposure. Emphysema developed after a 3-month CS exposure, accompanied by the recruitment of large numbers of macrophages to the lung. CS exposure substantially and persistently elevated the expression level of Smad7, resulting in a significant reduction of Smad2 phosphorylation (which controls MMP-9 expression) in Fut8(+/-) mice and Fut8-deficient embryonic fibroblast cells. These in vivo and in vitro studies show that impaired core fucosylation enhances the susceptibility to CS and constitutes at least part of the disease process of emphysema, in which TGF-β-Smad signaling is impaired and the MMP-mediated destruction of lung parenchyma is up-regulated.

Indexed as

AnimalsFucosyltransferasesGene Expression Regulation, EnzymologicHeterozygoteMatrix Metalloproteinase 9MiceMice, KnockoutPulmonary EmphysemaSignal TransductionSmad2 ProteinSmad7 ProteinTime FactorsTobacco Smoke PollutionTransforming Growth Factor betaFucosyltransferasesGlycoprotein 6-alpha-L-fucosyltransferaseMatrix Metalloproteinase 9Mmp9 protein, mouseSmad2 ProteinSmad2 protein, mouseSmad7 ProteinSmad7 protein, mouseTobacco Smoke PollutionTransforming Growth Factor beta

Identifiers

PMID22433854
PMCPMC3351343
OpenAlexW2082821300

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.