Evidence map›Paper›PMID 25820524›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015

Attenuating endogenous Fgfr2b ligands during bleomycin-induced lung fibrosis does not compromise murine lung repair.

BreAnne MacKenzie, Ingrid Henneke, Stefanie Hezel, Denise Al Alam, Elie El Agha, Cho-Ming Chao, Jennifer Quantius, Jochen Wilhelm, Matthew Jones, Kerstin Goth and 7 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Understanding myofibroblast origin in the fibrotic lung.Chinese medical journal pulmonary and critical care medicine · 2024
    Review
  5. Injury activated alveolar progenitors (IAAPs): the underdog of lung repair.Cellular and molecular life sciences : CMLS · 2023
    Review
  6. Review
  7. Article
  8. Anti-fibrotic effects of pharmacologic FGF-2: a review of recent literature.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. FGFR2 Is Required for AEC2 Homeostasis and Survival after Bleomycin-induced Lung Injury.American journal of respiratory cell and molecular biology · 2020
    Article
  15. Good Things Come in 2s: Type 2 Alveolar Epithelial Cells and Fibroblast Growth Factor Receptor 2.American journal of respiratory cell and molecular biology · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. 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

17 authors at 6 institutions in 4 countries.

BreAnne MacKenzieGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany;
Ingrid HennekeGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany;
Stefanie HezelGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany;
Denise Al AlamDevelopmental Biology Program, Division of Surgery, Saban Research Institute of Children's Hospital Los Angeles, University of Southern California Keck School of Medicine, Los Angeles, California;
Elie El AghaGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany;
Cho-Ming ChaoGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany;
Jennifer QuantiusGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany;
Jochen WilhelmGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany;
Matthew JonesGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany;
Kerstin GothGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany;
Xiaokun LiSchool of Pharmacy, Wenzhou Medical College, China;
Werner SeegerGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany;
Melanie KönigshoffComprehensive Pneumology Center, Ludwig Maximilians University, University Hospital Grosshadern, and Helmholtz Zentrum München, Munich, Bavaria, Germany;
Susanne HeroldGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany;
Albert A RizvanovInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Andreas GüntherGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany; AGAPLESION Lung Clinic Waldhof-Elgershausen, Greifenstein, Germany; German Center for Lung Research, Germany;
Saverio BellusciGerman Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany; Developmental Biology Program, Division of Surgery, Saban Research Institute of Children's Hospital Los Angeles, University of Southern California Keck School of Medicine, Los Angeles, California; Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia saverio.bellusci@innere.med.uni-giessen.de.
German Center for Lung Research · DEUniversities of Giessen and Marburg Lung Center · DEChildren's Hospital of Los Angeles · USHelmholtz Zentrum München · DEKazan Federal University · RUWenzhou Medical University · CN

Funding

MECHANISMS OF BPD PATHOGENESISR01HL107307 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MINOO, PARVIZ MINOO · 2012 to 2015
$1.6M
NHLBI NIH HHS R01 HL107307
6 · The paper itself

Abstract

Fibroblast growth factors (Fgfs) mediate organ repair. Lung epithelial cell overexpression of Fgf10 postbleomycin injury is both protective and therapeutic, characterized by increased survival and attenuated fibrosis. Exogenous administration of FGF7 (palifermin) also showed prophylactic survival benefits in mice. The role of endogenous Fgfr2b ligands on bleomycin-induced lung fibrosis is still elusive. This study reports the expression of endogenous Fgfr2b ligands, receptors, and signaling targets in wild-type mice following bleomycin lung injury. In addition, the impact of attenuating endogenous Fgfr2b-ligands following bleomycin-induced fibrosis was tested by using a doxycycline (dox)-based inducible, soluble, dominant-negative form of the Fgfr2b receptor. Double-transgenic (DTG) Rosa26(rtTA/+);tet(O)solFgfr2b mice were validated for the expression and activity of soluble Fgfr2b (failure to regenerate maxillary incisors, attenuated recombinant FGF7 signal in the lung). As previously reported, no defects in lung morphometry were detected in DTG (+dox) mice exposed from postnatal days (PN) 1 through PN105. Female single-transgenic (STG) and DTG mice were subjected to various levels of bleomycin injury (1.0, 2.0, and 3.0 U/kg). Fgfr2b ligands were attenuated either throughout injury (days 0-11; days 0-28) or during later stages (days 6-28 and 14-28). No significant changes in survival, weight, lung function, confluent areas of fibrosis, or hydroxyproline deposition were detected in DTG mice. These results indicate that endogenous Fgfr2b ligands do not significantly protect against bleomycin injury, nor do they expedite the resolution of bleomycin-induced lung injury in mice.

Indexed as

Pulmonary FibrosisAnimalsAntibiotics, AntineoplasticBleomycinFemaleFibroblast Growth Factor 7MiceMice, TransgenicReceptor, Fibroblast Growth Factor, Type 2Signal TransductionAntibiotics, AntineoplasticBleomycinFibroblast Growth Factor 7Receptor, Fibroblast Growth Factor, Type 2

Identifiers

PMID25820524
PMCPMC4437006
OpenAlexW1999825929

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.