Evidence map›Paper›PMID 24321990›Full record

ArticlePediatric research2014

Caffeine induces alveolar apoptosis in the hyperoxia-exposed developing mouse lung.

Sara Dayanim, Benjamin Lopez, Tiffany M Maisonet, Sungat Grewal, Vedang A Londhe

Open access · bronzeAbstract read
In one paragraph

Article in Pediatric research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
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  7. Apnea of prematurity and sudden infant death syndrome.Handbook of clinical neurology · 2022
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Caffeine and Clinical Outcomes in Premature Neonates.Children (Basel, Switzerland) · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Attenuation of endoplasmic reticulum stress by caffeine ameliorates hyperoxia-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2017
    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

5 authors at 1 institution in 1 country.

Sara DayanimDepartment of Pediatrics, Division of Neonatology and Developmental Biology, David Geffen School of Medicine, Neonatal Research Center, University of California, Los Angeles, California.
Benjamin LopezDepartment of Pediatrics, Division of Neonatology and Developmental Biology, David Geffen School of Medicine, Neonatal Research Center, University of California, Los Angeles, California.
Tiffany M MaisonetDepartment of Pediatrics, Division of Neonatology and Developmental Biology, David Geffen School of Medicine, Neonatal Research Center, University of California, Los Angeles, California.
Sungat GrewalDepartment of Pediatrics, Division of Neonatology and Developmental Biology, David Geffen School of Medicine, Neonatal Research Center, University of California, Los Angeles, California.
Vedang A LondheDepartment of Pediatrics, Division of Neonatology and Developmental Biology, David Geffen School of Medicine, Neonatal Research Center, University of California, Los Angeles, California.
University of California, Los Angeles · US

Funding

Inflammatory and Chemotactic Cytokines in Bronchopulmonary DysplasiaK08HL076538 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LONDHE, VEDANG A · 2007 to 2011
$609k
NHLBI NIH HHS HL076538NHLBI NIH HHS K08 HL076538
6 · The paper itself

Abstract

backgroundCaffeine is a nonspecific adenosine receptor antagonist used in premature neonates to treat apnea of prematurity. While its use may reduce the incidence of bronchopulmonary dysplasia (BPD), the precise mechanisms remain unknown. Evidence of increased adenosine levels are noted in chronic lung diseases including tracheal aspirates of infants with BPD. Utilizing a well-characterized newborn mouse model of alveolar hypoplasia, we hypothesized that hyperoxia-induced alveolar inflammation and hypoplasia is associated with alterations in the adenosine signaling pathway.

methodsNewborn murine pups were exposed to a 14-d period of hyperoxia and daily caffeine administration followed by a 14-d recovery period in room air. Lungs were collected at both time points for bronchoalveolar lavage (BAL) analysis as well as histopathology and mRNA and protein expression.

resultsCaffeine treatment increased inflammation and worsened alveolar hypoplasia in hyperoxia-exposed newborn mice. These changes were associated with decreased alveolar type II (ATII) cell numbers, increased cell apoptosis, and decreased expression of A2A receptors. Following discontinuation of caffeine and hyperoxia, lung histology returned to baseline levels comparable to hyperoxia exposure alone.

conclusionResults of this study suggest a potentially adverse role of caffeine on alveolar development in a murine model of hyperoxia-induced alveolar hypoplasia.

Indexed as

AdenosineAnimalsAnimals, NewbornApoptosisBronchoalveolar LavageCaffeineIn Situ Nick-End LabelingMicePulmonary AlveoliPurinergic P1 Receptor AntagonistsReceptor, Adenosine A2ASignal TransductionAdenosineCaffeinePurinergic P1 Receptor AntagonistsReceptor, Adenosine A2A

Identifiers

PMID24321990
PMCPMC3943688
OpenAlexW2005719144

What OpenQuestion holds

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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.