Evidence map›Paper›PMID 17316425›Full record

ArticleCritical care (London, England)2007

Hyperoxia increases ventilator-induced lung injury via mitogen-activated protein kinases: a prospective, controlled animal experiment.

Li-Fu Li, Shuen-Kuei Liao, Yu-Shien Ko, Cheng-Huei Lee, Deborah A Quinn

Open access · goldAbstract read
In one paragraph

Article in Critical care (London, England), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

73 citing papers in PubMed, 132 citations in OpenAlex.

  1. Bench evidence, bedside uncertainty: hyperoxia, mechanical ventilation and lung injury.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
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  13. Observational
  14. Dangers of hyperoxia.Critical care (London, England) · 2021
    Review
  15. Oxygen Toxicity in Critically Ill Adults.American journal of respiratory and critical care medicine · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

13 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 2 countries.

Li-Fu LiDivision of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, and Chang Gung University, Kweishan, Taoyuan 333, Taiwan. lfp3434@adm.cgmh.org.tw
Shuen-Kuei Liao
Yu-Shien Ko
Cheng-Huei Lee
Deborah A Quinn
Chang Gung University · TWChang Gung Memorial Hospital · TWMassachusetts General Hospital · USMemorial Hospital of South Bend · US

Funding

NHLBI NIH HHS HL039020
6 · The paper itself

Abstract

introductionLarge-tidal volume (VT) mechanical ventilation and hyperoxia used in patients with acute respiratory distress syndrome can damage pulmonary epithelial cells through lung inflammation and apoptotic cell death. Hyperoxia has been shown to increase ventilator-induced lung injury, but the mechanisms regulating interaction between large VT and hyperoxia are unclear. We hypothesized that the addition of hyperoxia to large-VT ventilation would increase neutrophil infiltration by upregulation of the cytokine macrophage inflammatory protein-2 (MIP-2) and would increase apoptosis via the mitogen-activated protein kinase pathways.

methodsC57BL/6 mice were exposed to high-VT (30 ml/kg) mechanical ventilation with room air or hyperoxia for one to five hours.

resultsThe addition of hyperoxia to high-VT ventilation augmented lung injury, as demonstrated by increased apoptotic cell death, neutrophil migration into the lung, MIP-2 production, MIP-2 mRNA expression, increased DNA binding activity of activator protein-1, increased microvascular permeability, and c-Jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) 1/2 activation. Hyperoxia-induced augmentation of high-VT-induced lung injury was attenuated in JNK-deficient mice and in mice with pharmacologic inhibition of ERK activity by PD98059. However, only JNK-deficient mice, and not mice with ERK activity inhibition by PD98059, were protected from high-VT-induced lung injury without hyperoxia.

conclusionWe conclude that hyperoxia increased high-VT-induced cytokine production, neutrophil influx, and apoptotic cell death through activation of the JNK and ERK1/2 pathways.

Indexed as

AnimalsApoptosisChemokine CXCL2CytokinesExtracellular Signal-Regulated MAP KinasesFlavonoidsHyperoxiaJNK Mitogen-Activated Protein KinasesLung DiseasesMiceMice, Inbred C57BLMice, KnockoutMonokinesNeutrophil InfiltrationRespiration, ArtificialRNA, Messenger2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneChemokine CXCL2CytokinesExtracellular Signal-Regulated MAP KinasesFlavonoidsJNK Mitogen-Activated Protein KinasesMonokinesRNA, Messenger

Identifiers

PMID17316425
PMCPMC2151853
OpenAlexW2128862148

What OpenQuestion holds

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LicenceCC BY
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.