Evidence map›Paper›PMID 15520863›Full record

ArticleThe Journal of clinical investigation2004

Imatinib mesylate inhibits the profibrogenic activity of TGF-beta and prevents bleomycin-mediated lung fibrosis.

Craig E Daniels, Mark C Wilkes, Maryanne Edens, Ted J Kottom, Stephen J Murphy, Andrew H Limper, Edward B Leof

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 258 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
258citing papers in PubMed, 1 pooled it
21.6field-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

258 citing papers in PubMed, 1 synthesis or guideline pooled it, 525 citations in OpenAlex.

  1. Guideline
  2. Trial
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  6. Article
  7. Review
  8. The critical role of LRG1 in pathological fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  9. Article
  10. Imaging technologies in experimental pulmonary fibrosis research: essential tool for enhanced translational relevance.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
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  18. Article
  19. Article
  20. Article

198 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Craig E DanielsThoracic Disease Research Unit, Division of Pulmonary and Critical Care Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.
Mark C Wilkes
Maryanne Edens
Ted J Kottom
Stephen J Murphy
Andrew H Limper
Edward B Leof
Mayo Clinic · USPulmonary and Critical Care Associates · US

Funding

TGF BETA RECEPTORS AND CELL PROLIFERATIONR01GM054200 · NIGMS · MAYO CLINIC ROCHESTER · PI LEOF, EDWARD B · 1996 to 2018
$6.1M
TGF Beta Receptor DynamicsR37GM055816 · NIGMS · MAYO CLINIC ROCHESTER · PI LEOF, EDWARD B · 2009 to 2018
$3.6M
TGF BETA RECEPTOR DYNAMICSR01GM055816 · NIGMS · MAYO CLINIC ROCHESTER · PI LEOF, EDWARD B · 1997 to 2008
$2.4M
NIGMS NIH HHS GM54200NIGMS NIH HHS GM55816NIGMS NIH HHS R01 GM054200NIGMS NIH HHS R01 GM055816NIGMS NIH HHS R37 GM055816
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis is a progressive and fatal fibrotic disease of the lungs with unclear etiology. Prior efforts to treat idiopathic pulmonary fibrosis that focused on anti-inflammatory therapy have not proven to be effective. Recent insight suggests that the pathogenesis is mediated through foci of dysregulated fibroblasts driven by profibrotic cytokine signaling. TGF-beta and PDGF are 2 of the most potent of these cytokines. In the current study, we investigated the role of TGF-beta-induced fibrosis mediated by activation of the Abelson (Abl) tyrosine kinase. Our data indicate that fibroblasts respond to TGF-beta by stimulating c-Abl kinase activity independently of Smad2/3 phosphorylation or PDGFR activation. Moreover, inhibition of c-Abl by imatinib prevented TGF-beta-induced ECM gene expression, morphologic transformation, and cell proliferation independently of any effect on Smad signaling. Further, using a mouse model of bleomycin-induced pulmonary fibrosis, we found a significant inhibition of lung fibrosis by imatinib. Thus, Abl family members represent common targets for the modulation of profibrotic cytokine signaling.

Indexed as

AnimalsAntineoplastic AgentsBenzamidesBleomycinBlotting, WesternCell ProliferationCells, CulturedCollagenCytokinesFibroblastsFibronectinsFibrosisImatinib MesylateImmunoprecipitationInflammationLuciferasesAntineoplastic AgentsBenzamidesBleomycinCollagenCytokinesFibronectinsImatinib MesylateLuciferasesPiperazinesProto-Oncogene Proteins c-ablPyrimidinesReceptors, Platelet-Derived Growth FactorTransforming Growth Factor betaTransforming Growth Factor beta2

Identifiers

PMID15520863
PMCPMC524221
OpenAlexW1977445008

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.