Evidence map›Paper›PMID 29345197›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018

Neonatal hyperoxia depletes pulmonary vein cardiomyocytes in adult mice via mitochondrial oxidation.

Min Yee, Ethan David Cohen, William Domm, George A Porter, Andrew N McDavid, Michael A O'Reilly

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.8field-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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Whole genome transcriptomics reveal distinct atrial versus ventricular responses to neonatal hyperoxia.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  4. Article
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  6. Low-dose hyperoxia primes airways for fibrosis in mice after influenza A infection.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  7. Article
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  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Swapping mitochondria: a key to understanding susceptibility to neonatal chronic lung disease.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  18. Review
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Min YeeDepartment of Pediatrics, School of Medicine and Dentistry, The University of Rochester , Rochester, New York.
Ethan David CohenDepartment of Medicine, School of Medicine and Dentistry, The University of Rochester , Rochester, New York.
William DommDepartment of Pediatrics, School of Medicine and Dentistry, The University of Rochester , Rochester, New York.
George A PorterDepartment of Pediatrics, School of Medicine and Dentistry, The University of Rochester , Rochester, New York.
Andrew N McDavidBiostatistics and Computational Biology, School of Medicine and Dentistry, The University of Rochester , Rochester, New York.
Michael A O'Reilly
University of Rochester · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Martha Susiarjo · 1985 to 2026
$42.8M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
Effect of Neonatal Hyperoxia on Alveolar Development and InfectionR01HL091968 · NHLBI · UNIVERSITY OF ROCHESTER · PI O'REILLY, MICHAEL A · 2009 to 2021
$5.4M
NHLBI NIH HHS R01 HL091968NIEHS NIH HHS P30 ES001247NIEHS NIH HHS T32 ES007026
6 · The paper itself

Abstract

Supplemental oxygen given to preterm infants has been associated with permanently altering postnatal lung development. Now that these individuals are reaching adulthood, there is growing concern that early life oxygen exposure may also promote cardiovascular disease through poorly understood mechanisms. We previously reported that adult mice exposed to 100% oxygen between postnatal days 0 and 4 develop pulmonary hypertension, defined pathologically by capillary rarefaction, dilation of arterioles and veins, cardiac failure, and a reduced lifespan. Here, Affymetrix Gene Arrays are used to identify early transcriptional changes that take place in the lung before pulmonary capillary rarefaction. We discovered neonatal hyperoxia reduced expression of cardiac muscle genes, including those involved in contraction, calcium signaling, mitochondrial respiration, and vasodilation. Quantitative RT-PCR, immunohistochemistry, and genetic lineage mapping using Myh6

Indexed as

AnimalsAnimals, NewbornBiomarkersCells, CulturedGene Expression ProfilingHyperoxiaHypertension, PulmonaryMaleMiceMice, Inbred C57BLMitochondriaMyocytes, CardiacOxidation-ReductionOxygenPulmonary VeinsBiomarkersOxygencardiomyocyteshyperoxiapretermpulmonary hypertension

Identifiers

PMID29345197
PMCPMC6008126
OpenAlexW2782627216

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.