Evidence map›Paper›PMID 24024157›Full record

ArticleRedox biology2013

Heme oxygenase-1 regulates postnatal lung repair after hyperoxia: role of β-catenin/hnRNPK signaling.

Guang Yang, Chhanda Biswasa, Qing Sara Lin, Ping La, Fumihiko Namba, Tiangang Zhuang, Manasa Muthu, Phyllis A Dennery

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. The Role of Heme Oxygenase-1 Promoter Polymorphisms in Perinatal Disease.International journal of environmental research and public health · 2021
    Pooled it
  2. Review
  3. Article
  4. Association ofBiomedicines · 2025
    Article
  5. Article
  6. Article
  7. Oxidative Stress in Fetuses and Newborns.Antioxidants (Basel, Switzerland) · 2024
    Article
  8. Heme Oxygenase-1 and Its Role in Colorectal Cancer.Antioxidants (Basel, Switzerland) · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Heme Oxygenase 1 in Vertebrates: Friend and Foe.Cell biochemistry and biophysics · 2022
    Review
  13. The Nuclear Translocation of Heme Oxygenase-1 in Human Diseases.Frontiers in cell and developmental biology · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Interactive and independent effects of early lipopolysaccharide and hyperoxia exposure on developing murine lungs.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

Guang YangDivision of Neonatology, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
Chhanda Biswasa
Qing Sara Lin
Ping La
Fumihiko Namba
Tiangang Zhuang
Manasa Muthu
Phyllis A Dennery
Children's Hospital of Philadelphia · USUniversity of Pennsylvania · US

Funding

Role of Heme Oxygenase in Neonatal Hyperoxic InjuryR01HL058752 · NHLBI · STANFORD UNIVERSITY · PI DENNERY, PHYLLIS A. · 1999 to 2013
$4.5M
NHLBI NIH HHS HL-058752NHLBI NIH HHS R01 HL058752
6 · The paper itself

Abstract

In the newborn, alveolarization continues postnatally and can be disrupted by hyperoxia, leading to long-lasting consequences on lung function. We wanted to better understand the role of heme oxygenase (HO)-1, the inducible form of the rate-limiting enzyme in heme degradation, in neonatal hyperoxic lung injury and repair. Although it was not observed after 3 days of hyperoxia alone, when exposed to hyperoxia and allowed to recover in air (O2/air recovered), neonatal HO-1 knockout (KO) mice had enlarged alveolar spaces and increased lung apoptosis as well as decreased lung protein translation and dysregulated gene expression in the recovery phase of the injury. Associated with these changes, KO had sustained low levels of active β-catenin and lesser lung nuclear heterogeneous nuclear ribonucleoprotein K (hnRNPK) protein levels, whereas lung nuclear hnRNPK was increased in transgenic mice over-expressing nuclear HO-1. Disruption of HO-1 may enhance hnRNPK-mediated inhibition of protein translation and subsequently impair the β-catenin/hnRNPK regulated gene expression required for coordinated lung repair and regeneration.

Indexed as

AnimalsAnimals, Newbornbeta CateninCell LineCell NucleusGene Expression RegulationGene Knockout TechniquesHeme Oxygenase-1Heterogeneous-Nuclear Ribonucleoprotein KHyperoxiaLungLung InjuryMembrane ProteinsMiceMice, Inbred C57BLRibonucleoproteinsbeta CateninHeme Oxygenase-1Heterogeneous-Nuclear Ribonucleoprotein KHmox1 protein, mouseHNRNPK protein, mouseMembrane ProteinsRibonucleoproteinsCell proliferationDNA damage and repairHeme oxygenase-1hnRNPK, heterogeneous nuclear ribonucleoprotein protein KHO-1, heme oxygenase-1KO, knockoutMEF, mouse embryonic fibroblastsNeonatal hyperoxic lung injury and repairO2/air, exposed to 95% oxygen for 3 days then recovered in airOGG1, 8-oxoguanine DNA glycosylaseRAC, radial alveolar countsSP-B, surfactant protein BSP-C, surfactant protein Cβ-catenin/hnRNPK

Identifiers

PMID24024157
PMCPMC3757689
OpenAlexW2027123502

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.