Evidence map›Paper›PMID 28487375›Full record

ArticleThe Journal of biological chemistry2017

Pulmonary fibrosis requires cell-autonomous mesenchymal fibroblast growth factor (FGF) signaling.

Robert D Guzy, Ling Li, Craig Smith, Samuel J Dorry, Hyun Young Koo, Lin Chen, David M Ornitz

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 71 citations in OpenAlex.

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  8. Pharmaceuticals (Basel, Switzerland) · 2025
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  17. Anti-fibrotic effects of pharmacologic FGF-2: a review of recent literature.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
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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

7 authors at 3 institutions in 2 countries.

Robert D GuzyFrom the Department of Medicine, Section of Pulmonary and Critical Care Medicine, The University of Chicago, Chicago, Illinois 60637, rguzy1@bsd.uchicago.edu.ORCID 0000-0001-8420-6177
Ling Lithe Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri 63110, and.
Craig Smiththe Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri 63110, and.
Samuel J DorryFrom the Department of Medicine, Section of Pulmonary and Critical Care Medicine, The University of Chicago, Chicago, Illinois 60637.
Hyun Young KooFrom the Department of Medicine, Section of Pulmonary and Critical Care Medicine, The University of Chicago, Chicago, Illinois 60637.
Lin Chenthe Department of Rehabilitation Medicine, Center of Bone Metabolism and Repair, State Key Laboratory of Trauma, Burns, and Combined Injury, Daping Hospital, Third Military Medical University, Chongqing 400042, China.
David M Ornitzthe Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri 63110, and.ORCID 0000-0003-1592-7629
Washington University in St. Louis · USUniversity of Chicago · USArmy Medical University · CN

Funding

PRINCIPLES IN PULMONARY RESEARCHT32HL007317 · NHLBI · WASHINGTON UNIVERSITY · PI Steven Brody, Michael J Holtzman · 1985 to 2026
$16.1M
REGULATION OF LUNG DEVELOPMENT BY FGF9 SIGNALING PATHWAYSR01HL111190 · NHLBI · WASHINGTON UNIVERSITY · PI ORNITZ, DAVID M · 2012 to 2020
$3.9M
Mechanism of Fibroblast Growth Factor 2-Mediated Alveolar Epithelial RepairK08HL125910 · NHLBI · UNIVERSITY OF CHICAGO · PI GUZY, ROBERT DAVID · 2017 to 2021
$820k
WHOLE SLIDE IMAGING SYSTEM FOR TRANSLATIONAL NEUROSCIENCES10RR027552 · NCRR · WASHINGTON UNIVERSITY · PI LEE, JIN-MOO · 2010 to 2010
$275k
NCRR NIH HHS S10 RR027552NHLBI NIH HHS K08 HL125910NHLBI NIH HHS R01 HL111190NHLBI NIH HHS T32 HL007317
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is characterized by progressive pulmonary scarring, decline in lung function, and often results in death within 3-5 five years after diagnosis. Fibroblast growth factor (FGF) signaling has been implicated in the pathogenesis of IPF; however, the mechanism through which FGF signaling contributes to pulmonary fibrosis remains unclear. We hypothesized that FGF receptor (FGFR) signaling in fibroblasts is required for the fibrotic response to bleomycin. To test this, mice with mesenchyme-specific tamoxifen-inducible inactivation of FGF receptors 1, 2, and 3 (

Indexed as

AnimalsBleomycinCollagen Type IEpidermal Growth FactorMiceMice, KnockoutPulmonary FibrosisReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 2Receptor, Fibroblast Growth Factor, Type 3Signal TransductionBleomycinCol1a2 protein, mouseCollagen Type IEpidermal Growth FactorFgfr1 protein, mouseFgfr2 protein, mouseFgfr3 protein, mouseReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 2Receptor, Fibroblast Growth Factor, Type 3bleomycincollagenfibroblastfibroblast growth factor (FGF)fibroblast growth factor receptor (FGFR)lung injurymyofibroblastpulmonary fibrosis

Identifiers

PMID28487375
PMCPMC5481550
OpenAlexW2612572443

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.