Evidence map›Paper›PMID 24325475›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

Targeting interleukin-13 with tralokinumab attenuates lung fibrosis and epithelial damage in a humanized SCID idiopathic pulmonary fibrosis model.

Lynne A Murray, Huilan Zhang, Sameer R Oak, Ana Lucia Coelho, Athula Herath, Kevin R Flaherty, Joyce Lee, Matt Bell, Darryl A Knight, Fernando J Martinez and 3 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
12.3field-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

54 citing papers in PubMed, 115 citations in OpenAlex.

  1. Trial
  2. Mechanosignaling through YAP and TAZ drives fibroblast activation and fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2015
    Trial
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Leukemia inhibitory factor (LIF) receptor amplifies pathogenic activation of fibroblasts in lung fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. The role of inflammation in silicosis.Frontiers in pharmacology · 2024
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Observational
  19. Review
  20. Review
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

13 authors at 6 institutions in 3 countries.

Lynne A Murray1 MedImmune Ltd, Cambridge, United Kingdom.
Huilan Zhang
Sameer R Oak
Ana Lucia Coelho
Athula Herath
Kevin R Flaherty
Joyce Lee
Matt Bell
Darryl A Knight
Fernando J Martinez
Matthew A Sleeman
Erica L Herzog
Cory M Hogaboam
University of Michigan · USAimmune Therapeutics (United Kingdom) · GBMichigan Medicine · USUniversity of British Columbia · CAUniversity of California, San Francisco · USYale University · US

Funding

CTRIP: Molecular phenotypes of rapidly progressive idiopathic pulmonary fibrosisRC2HL101740 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FLAHERTY, KEVIN R, MARTINEZ, FERNANDO J · 2009 to 2010
$7.9M
Novel Immunologic Effects of Semaphorin 7a in IPFR01HL109233 · NHLBI · YALE UNIVERSITY · PI HERZOG, ERICA L · 2011 to 2019
$3.7M
Forging a road to personalized medicine in interstitial lung diseasesK24HL111316 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FLAHERTY, KEVIN R · 2012 to 2017
$909k
NHLBI NIH HHS HL109033NHLBI NIH HHS K24 HL111316NHLBI NIH HHS R01 HL109233NHLBI NIH HHS RC2 HL101740
6 · The paper itself

Abstract

The aberrant fibrotic and repair responses in the lung are major hallmarks of idiopathic pulmonary fibrosis (IPF). Numerous antifibrotic strategies have been used in the clinic with limited success, raising the possibility that an effective therapeutic strategy in this disease must inhibit fibrosis and promote appropriate lung repair mechanisms. IL-13 represents an attractive target in IPF, but its disease association and mechanism of action remains unknown. In the present study, an overexpression of IL-13 and IL-13 pathway markers was associated with IPF, particularly a rapidly progressive form of this disease. Targeting IL-13 in a humanized experimental model of pulmonary fibrosis using tralokinumab (CAT354) was found to therapeutically block aberrant lung remodeling in this model. However, targeting IL-13 was also found to promote lung repair and to restore epithelial integrity. Thus, targeting IL-13 inhibits fibrotic processes and enhances repair processes in the lung.

Indexed as

AnimalsAntibodies, MonoclonalEpithelial CellsFemaleHumansIdiopathic Pulmonary FibrosisInterleukin-13LungMiceMice, SCIDMolecular Targeted TherapyUp-RegulationAntibodies, MonoclonalInterleukin-13tralokinumab

Identifiers

PMID24325475
PMCPMC4068948
OpenAlexW2078995879

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.