Evidence map›Paper›PMID 25275225›Full record

ArticleAmerican journal of respiratory cell and molecular biology2015

Foxm1 regulates resolution of hyperoxic lung injury in newborns.

Hongping Xia, Xiaomeng Ren, Craig S Bolte, Vladimir Ustiyan, Yufang Zhang, Tushar A Shah, Tanya V Kalin, Jeffrey A Whitsett, Vladimir V Kalinichenko

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2015. 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
2.2field-weighted citation impact, top 13% 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. Review
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  4. Review
  5. Review
  6. CRISPR-Cas9 Genome Editing Allows Generation of the Mouse Lung in a Rat.American journal of respiratory and critical care medicine · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. The role of FoxM1 in immune cells.Clinical and experimental medicine · 2023
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Therapeutic Potential of Endothelial Progenitor Cells in Pulmonary Diseases.American journal of respiratory cell and molecular biology · 2021
    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

9 authors at 1 institution in 2 countries.

Hongping Xia3 Division of Neonatology and Pulmonary Biology.
Xiaomeng Ren
Craig S Bolte
Vladimir Ustiyan
Yufang Zhang
Tushar A Shah
Tanya V Kalin
Jeffrey A Whitsett
Vladimir V Kalinichenko
Cincinnati Children's Hospital Medical Center · US

Funding

Fox Transcription Factors in Development of Pulmonary CapillariesR01HL084151 · NHLBI · UNIVERSITY OF CHICAGO · PI KALINICHENKO, VLADIMIR · 2006 to 2018
$4.9M
"Lung MAP" Atlas Research CenterU01HL122642 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI POTTER, S. STEVEN, WHITSETT, JEFFREY A · 2014 to 2018
$3.9M
Transcriptional regulation of goblet cell metaplasiaR01HL123490 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI KALINICHENKO, VLADIMIR · 2014 to 2017
$1.6M
Role of Foxm1 in Lung Cancer MicroenvironmentR01CA142724 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI KALIN, TANYA · 2010 to 2014
$1.5M
NCI NIH HHS CA142724NCI NIH HHS R01 CA142724NHLBI NIH HHS HL123490NHLBI NIH HHS HL84151NHLBI NIH HHS R01 HL084151NHLBI NIH HHS R01 HL123490NHLBI NIH HHS U01 HL122642
6 · The paper itself

Abstract

Current treatments for inflammation associated with bronchopulmonary dysplasia (BPD) fail to show clinical efficacy. Foxm1, a transcription factor of the Forkhead box family, is a critical mediator of lung development and carcinogenesis, but its role in BPD-associated pulmonary inflammation is unknown. Immunohistochemistry and RNA analysis were used to assess Foxm1 in lung tissue from hyperoxia-treated mice and patients with BPD. LysM-Cre/Foxm1(-/-) mice, in which Foxm1 was deleted from myeloid-derived inflammatory cells, including macrophages, monocytes, and neutrophils, were exposed to neonatal hyperoxia, causing lung injury and remodeling. Measurements of lung function and flow cytometry were used to evaluate the effects of Foxm1 deletion on pulmonary inflammation and repair. Increased Foxm1 expression was observed in pulmonary macrophages of hyperoxia-exposed mice and in lung tissue from patients with BPD. After hyperoxia, deletion of Foxm1 from the myeloid cell lineage decreased numbers of interstitial macrophages (CD45(+)CD11b(+)Ly6C(-)Ly6G(-)F4/80(+)CD68(-)) and impaired alveologenesis and lung function. The exaggerated BPD-like phenotype observed in hyperoxia-exposed LysM-Cre/Foxm1(-/-) mice was associated with increased expression of neutrophil-derived myeloperoxidase, proteinase 3, and cathepsin g, all of which are critical for lung remodeling and inflammation. Our data demonstrate that Foxm1 influences pulmonary inflammatory responses to hyperoxia, inhibiting neutrophil-derived enzymes and enhancing monocytic responses that limit alveolar injury and remodeling in neonatal lungs.

Indexed as

Airway RemodelingAlveolar Epithelial CellsAnimalsBronchopulmonary DysplasiaCase-Control StudiesCathepsin GDisease Models, AnimalForkhead Box Protein M1Forkhead Transcription FactorsHumansHyperoxiaInfant, NewbornLungLung InjuryMacrophagesMice, KnockoutCathepsin GCtsg protein, mouseForkhead Box Protein M1Forkhead Transcription FactorsFOXM1 protein, humanFoxm1 protein, mouseMyeloblastinPeroxidasebronchopulmonary dysplasiaFoxm1hyperoxiainflammationmacrophage

Identifiers

PMID25275225
PMCPMC4491137
OpenAlexW1998733491

What OpenQuestion holds

Textmetadata
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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.