Evidence map›Paper›PMID 31860803›Full record

ArticleAmerican journal of respiratory cell and molecular biology2020

FGFR2 Is Required for AEC2 Homeostasis and Survival after Bleomycin-induced Lung Injury.

Samuel J Dorry, Brandon O Ansbro, David M Ornitz, Gökhan M Mutlu, Robert D Guzy

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Genetic Strategies for Labeling AT2 Cells in Murine Lung via Abca3 and Etv5-Driven Reporters.Journal of respiratory biology and translational medicine · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Cell Cross-Talk in Alveolar Microenvironment: From Lung Injury to Fibrosis.American journal of respiratory cell and molecular biology · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Injury activated alveolar progenitors (IAAPs): the underdog of lung repair.Cellular and molecular life sciences : CMLS · 2023
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Samuel J DorrySection of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Chicago, Illinois; and.
Brandon O AnsbroSection of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Chicago, Illinois; and.
David M OrnitzDepartment of Developmental Biology, Washington University in St. Louis, St. Louis, Missouri.
Gökhan M MutluSection of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Chicago, Illinois; and.ORCID 0000-0002-2056-612X
Robert D GuzySection of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Chicago, Illinois; and.ORCID 0000-0001-8420-6177
University of Chicago · USWashington University in St. Louis · US

Funding

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
NHLBI NIH HHS K08 HL125910NHLBI NIH HHS R01 HL111190
6 · The paper itself

Abstract

Alveolar epithelial cell (AEC) injury is central to the pathogenesis of pulmonary fibrosis. Epithelial FGF (fibroblast growth factor) signaling is essential for recovery from hyperoxia- and influenza-induced lung injury, and treatment with FGFs is protective in experimental lung injury. The cell types involved in the protective effect of FGFs are not known. We hypothesized that FGF signaling in type II AECs (AEC2s) is critical in bleomycin-induced lung injury and fibrosis. To test this hypothesis, we generated mice with tamoxifen-inducible deletion of FGFR1-3 (fibroblast growth factor receptors 1, 2, and 3) in surfactant protein C-positive (SPC

Indexed as

HomeostasisAnimalsBleomycinCell LineageCollagenGene DeletionGene Expression RegulationLung InjuryMice, KnockoutOrgan SpecificityPhenotypePulmonary AlveoliPulmonary Surfactant-Associated Protein CReceptor, Fibroblast Growth Factor, Type 2Survival AnalysisBleomycinCollagenFgfr2 protein, mousePulmonary Surfactant-Associated Protein CReceptor, Fibroblast Growth Factor, Type 2alveolar epithelial cellsbleomycinfibroblast growth factorfibroblast growth factor receptorlung injury

Identifiers

PMID31860803
PMCPMC7193788
OpenAlexW2996377481

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.