Evidence map›Paper›PMID 28438602›Full record

ArticleBiochemical and biophysical research communications2017

Hyperoxia exposure disrupts adrenomedullin signaling in newborn mice: Implications for lung development in premature infants.

Renuka T Menon, Amrit Kumar Shrestha, Binoy Shivanna

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Protective effect of adrenomedullin on hyperoxia-induced lung injury.Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2021
    Article
  7. EndothelialAntioxidants (Basel, Switzerland) · 2021
    Article
  8. Review
  9. Article
  10. Inhibition of TGF-β-Smad signaling attenuates hyperoxia-induced brain damage in newborn rats.International journal of clinical and experimental pathology · 2019
    Article
  11. Article
  12. Lung omics signatures in a bronchopulmonary dysplasia and pulmonary hypertension-like murine model.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  13. Article
  14. Long-term pulmonary and cardiovascular morbidities of neonatal hyperoxia exposure in mice.The international journal of biochemistry & cell biology · 2018
    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

3 authors at 2 institutions in 1 country.

Renuka T MenonSection of Neonatology, Department of Pediatrics, Texas Children's Hospital, Baylor College of Medicine, Houston, TX 77030, United States.
Amrit Kumar ShresthaSection of Neonatology, Department of Pediatrics, Texas Children's Hospital, Baylor College of Medicine, Houston, TX 77030, United States.
Binoy ShivannaSection of Neonatology, Department of Pediatrics, Texas Children's Hospital, Baylor College of Medicine, Houston, TX 77030, United States. Electronic address: shivanna@bcm.edu.
Texas Children's Hospital · USBaylor College of Medicine · US

Funding

Tissue Analysis & Molecular Imaging CoreP30DK056338 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI Geoffrey A Preidis · 2001 to 2026
$28.3M
Modulation of Neonatal Hyperoxic Lung Injury by the Aryl Hydrocarbon ReceptorK08HD073323 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI SHIVANNA, BINOY · 2013 to 2017
$649k
NICHD NIH HHS K08 HD073323NIDDK NIH HHS P30 DK056338
6 · The paper itself

Abstract

Hyperoxia contributes to the development of bronchopulmonary dysplasia (BPD), a chronic lung disease of human infants that is characterized by disrupted lung angiogenesis. Adrenomedullin (AM) is a multifunctional peptide with angiogenic and vasoprotective properties. AM signals via its cognate receptors, calcitonin receptor-like receptor (Calcrl) and receptor activity-modifying protein 2 (RAMP2). Whether hyperoxia affects the pulmonary AM signaling pathway in neonatal mice and whether AM promotes lung angiogenesis in human infants are unknown. Therefore, we tested the following hypotheses: (1) hyperoxia exposure will disrupt AM signaling during the lung development period in neonatal mice; and (2) AM will promote angiogenesis in fetal human pulmonary artery endothelial cells (HPAECs) via extracellular signal-regulated kinases (ERK) 1/2 activation. We initially determined AM, Calcrl, and RAMP2 mRNA levels in mouse lungs on postnatal days (PND) 3, 7, 14, and 28. Next we determined the mRNA expression of these genes in neonatal mice exposed to hyperoxia (70% O

Indexed as

Signal TransductionAdrenomedullinAnimalsAnimals, NewbornHumansHyperoxiaInfant, NewbornInfant, PrematureLungMiceReceptors, AdrenomedullinAdrenomedullinReceptors, AdrenomedullinAdrenomedullinBronchopulmonary dysplasiaCalcitonin receptor-like receptorHyperoxiaReceptor activity-modifying protein 2

Identifiers

PMID28438602
PMCPMC5497733
OpenAlexW2607241477

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.