Evidence map›Paper›PMID 29308441›Full record

ArticleCurrent opinion in toxicology2018

Oxidative Stress in the Lung - The Essential Paradox.

Lynette K Rogers, Mary J Cismowski

Abstract read
In one paragraph

Article in Current opinion in toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 2 pooled it
9.2field-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

61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 143 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Microbiology spectrum · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Characterization of woodsmoke generated in the air pollution exposure lab and comparison to diesel exhaust.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  8. Article
  9. Review
  10. Review
  11. Ferroptosis surveillance: Insights fromFerroptosis and oxidative stress · 2026
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Elevated Senescence Markers in Developing Trisomy 21 Human Lungs.American journal of respiratory cell and molecular biology · 2025
    Article
  19. Article
  20. Article

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

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

2 authors at 2 institutions in 1 country.

Lynette K RogersCenter for Perinatal Research, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus Ohio.
Mary J CismowskiCenter for Cardiovascular Research, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus Ohio.
Nationwide Children's Hospital · USThe Ohio State University · US

Funding

DHA attenuates Inflammatory Responses Through Altering RAGE SignalingR01AT006880 · NCCIH · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI ROGERS, LYNETTE KAY · 2011 to 2015
$1.8M
Optimizing Therapeutic delivery of MicroRNAs to prevent chronic lung disease in Preterm infants.R01HD088033 · NICHD · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI ROGERS, LYNETTE KAY · 2017 to 2021
$1.6M
NCCIH NIH HHS R01 AT006880NICHD NIH HHS R01 HD088033
6 · The paper itself

Abstract

As eukaryotic life evolved, so too did the need for a source of energy that meets the requirements of complex organisms. Oxygen provides this vast potential energy source, but the same chemical reactivity which provides this potential also can have detrimental effects. The lung evolved as an organ that can efficiently promote gas exchange for the entire organism but as such, the lung is highly susceptible to its external environment. Oxygen can be transformed through both enzymatic and non-enzymatic processes into reactive oxygen species (ROS) and reactive nitrogen species (RNS), which can lead to protein, lipid, and DNA damage. Under normal conditions ROS/RNS concentrations are minimized through the activity of antioxidants located both intracellularly and in the epithelial lining fluid of the lung. Oxidative stress in the lung results when the antioxidant capacity is overwhelmed or depleted through external exposures, such as altered oxygen tension or air pollution, or internally. Internal sources of oxidative stress include systemic disease and the activation of resident cells and inflammatory cells recruited in response to an exposure or systemic response. Pulmonary responses to oxidative stress include activation of oxidases, lipid peroxidation, increases in nitric oxide, and autophagy. These internal and external exposures with the subsequent pulmonary responses contribute to development of diseases directly linked to oxidative stress. These include asthma, COPD, and lung cancers. While the vulnerability of the lung to oxidative stress is acknowledged, few effective preventative strategies or therapeutics are currently available.

Identifiers

PMID29308441
PMCPMC5754020
OpenAlexW2755788236

What OpenQuestion holds

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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.