Evidence map›Paper›PMID 10393853›Full record

ArticleThe American journal of pathology1999

Specific inhibitors of platelet-derived growth factor or epidermal growth factor receptor tyrosine kinase reduce pulmonary fibrosis in rats.

A B Rice, C R Moomaw, D L Morgan, J C Bonner

Open access · greenAbstract read
In one paragraph

Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 143 citations in OpenAlex.

  1. Trial
  2. Investigating the therapeutic role of anlotinib in radiation-induced lung injury.Naunyn-Schmiedeberg's archives of pharmacology · 2025
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  15. Targeting the PDGF signaling pathway in the treatment of non-malignant diseases.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014
    Article
  16. Article
  17. Profibrotic TGFβ responses require the cooperative action of PDGF and ErbB receptor tyrosine kinases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    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

4 authors at 2 institutions in 1 country.

A B RiceLaboratories of Pulmonary Pathobiology, Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
C R Moomaw
D L Morgan
J C Bonner
National Institute of Environmental Health Sciences · USTriangle · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The proliferation of myofibroblasts is a central feature of pulmonary fibrosis. In this study we have used tyrosine kinase inhibitors of the tyrphostin class to specifically block autophosphorylation of the platelet-derived growth factor receptor (PDGF-R) or epidermal growth factor receptor (EGF-R). AG1296 specifically inhibited autophosphorylation of PDGF-R and blocked PDGF-stimulated [3H]thymidine uptake by rat lung myofibroblasts in vitro. AG1478 was demonstrated as a selective blocker of EGF-R autophosphorylation and inhibited EGF-stimulated DNA synthesis in vitro. In a rat model of pulmonary fibrosis caused by intratracheal instillation of vanadium pentoxide (V2O5), intraperitoneal delivery of 50 mg/kg AG1296 or AG1478 in dimethylsulfoxide 1 hour before V2O5 instillation and again 2 days after instillation reduced the number of epithelial and mesenchymal cells incorporating bromodeoxyuridine (Brdu) by approximately 50% at 3 and 6 days after instillation. V2O5 instillation increased lung hydroxyproline fivefold 15 days after instillation, and AG1296 was more than 90% effective in preventing the increase in hydroxyproline, whereas AG1478 caused a 50% to 60% decrease in V2O5-stimulated hydroxyproline accumulation. These data provide evidence that PDGF and EGF receptor ligands are potent mitogens for collagen-producing mesenchymal cells during pulmonary fibrogenesis, and targeting tyrosine kinase receptors could offer a strategy for the treatment of fibrotic lung diseases.

Indexed as

AnimalsCollagenEnzyme InhibitorsErbB ReceptorsLungMitosisPhosphorylationPulmonary FibrosisQuinazolinesRatsRats, Sprague-DawleyReceptor Protein-Tyrosine KinasesReceptors, Platelet-Derived Growth FactorTyrphostins6,7-dimethoxy-3-phenylquinoxalineCollagenEnzyme InhibitorsErbB ReceptorsQuinazolinesReceptor Protein-Tyrosine KinasesReceptors, Platelet-Derived Growth FactorRTKI cpdTyrphostins

Identifiers

PMID10393853
PMCPMC1866660
OpenAlexW1972644785

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.