Evidence map›Paper›PMID 17349918›Full record

ReviewFree radical biology & medicine2007

Hyperoxia-induced signal transduction pathways in pulmonary epithelial cells.

Tahereh E Zaher, Edmund J Miller, Dympna M P Morrow, Mohammad Javdan, Lin L Mantell

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 6% 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

56 citing papers in PubMed, 2 syntheses or guidelines pooled it, 135 citations in OpenAlex.

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  16. Oxidative stress diseases unique to the perinatal period: A window into the developing innate immune response.American journal of reproductive immunology (New York, N.Y. : 1989) · 2018
    Review
  17. Akap1 genetic deletion increases the severity of hyperoxia-induced acute lung injury in mice.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  18. Article
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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

5 authors at 3 institutions in 1 country.

Tahereh E ZaherDepartment of Pharmaceutical Sciences, St. John's University College of Pharmacy, Queens, NY 11439, USA.
Edmund J Miller
Dympna M P Morrow
Mohammad Javdan
Lin L Mantell
Feinstein Institute for Medical Research · USSt. John's University · USNorthwell Health · US

Funding

The Lung as a Source of Inflammation in SepsisR01HL081655 · NHLBI · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI MILLER, EDMUND J · 2006 to 2009
$1.6M
NHLBI NIH HHS R01 HL081655
6 · The paper itself

Abstract

Mechanical ventilation with hyperoxia is necessary to treat critically ill patients. However, prolonged exposure to hyperoxia leads to the generation of excessive reactive oxygen species (ROS), which can cause acute inflammatory lung injury. One of the major effects of hyperoxia is the injury and death of pulmonary epithelium, which is accompanied by increased levels of pulmonary proinflammatory cytokines and excessive leukocyte infiltration. A thorough understanding of the signaling pathways leading to pulmonary epithelial cell injury/death may provide some insights into the pathogenesis of hyperoxia-induced acute inflammatory lung injury. This review focuses on epithelial responses to hyperoxia and some of the major factors regulating pathways to epithelial cell injury/death, and proinflammatory responses on exposure to hyperoxia. We discuss in detail some of the most interesting players, such as NF-kappaB, that can modulate both proinflammatory responses and cell injury/death of lung epithelial cells. A better appreciation for the functions of these factors will no doubt help us to delineate the pathways to hyperoxic cell death and proinflammatory responses.

Indexed as

Signal TransductionAnimalsCell DeathCytokinesEpithelial CellsGene ExpressionHumansHyperoxiaLungReactive Oxygen SpeciesTranscription FactorsCytokinesReactive Oxygen SpeciesTranscription Factors

Identifiers

PMID17349918
PMCPMC1876680
OpenAlexW1988662519

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.