Evidence map›Paper›PMID 37395632›Full record

ArticlePhysiological genomics2023

Endothelial to mesenchymal transition in neonatal hyperoxic lung injury: role of sex as a biological variable.

Abiud Cantu, Manuel Cantu Gutierrez, Yuhao Zhang, Xiaoyu Dong, Krithika Lingappan

Open access · greenAbstract read
In one paragraph

Article in Physiological genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Isoform-Specific Roles of NTRK2 in Pulmonary Vascular Regeneration.bioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Exogenous hydrogen sulfide attenuates hyperoxia effects on neonatal mouse airways.American journal of physiology. Lung cellular and molecular physiology · 2024
    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 2 institutions in 1 country.

Abiud CantuDivision of Neonatology, Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States.ORCID 0000-0003-0069-2134
Manuel Cantu GutierrezDivision of Neonatology, Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States.ORCID 0000-0002-1942-3316
Yuhao ZhangDivision of Neonatology, Department of Pediatrics, Texas Children's Hospital, Baylor College of Medicine, Houston, Texas, United States.
Xiaoyu DongDivision of Neonatology, Department of Pediatrics, Texas Children's Hospital, Baylor College of Medicine, Houston, Texas, United States.
Krithika LingappanDivision of Neonatology, Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States.ORCID 0000-0003-0821-2289
Children's Hospital of Philadelphia · USBaylor College of Medicine · US

Funding

Mechanisms of sex differences in neonatal pulmonary oxygen toxicityR01HL144775 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI LINGAPPAN, KRITHIKA · 2019 to 2023
$2.7M
Leveraging multiomics and advanced mouse models to delineate mechanisms underlying sex‐specific differences in recovery and repair after neonatal hyperoxia exposure in the developing lungR01HL146395 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI LINGAPPAN, KRITHIKA · 2020 to 2023
$1.6M
NHLBI NIH HHS HL144775NHLBI NIH HHS HL146395NHLBI NIH HHS R01 HL144775NHLBI NIH HHS R01 HL146395
6 · The paper itself

Abstract

Bronchopulmonary dysplasia (BPD) is characterized by an arrest in alveolarization, abnormal vascular development, and variable interstitial fibroproliferation in the premature lung. Endothelial to mesenchymal transition (EndoMT) may be a source of pathological fibrosis in many organ systems. Whether EndoMT contributes to the pathogenesis of BPD is not known. We tested the hypothesis that pulmonary endothelial cells will show increased expression of EndoMT markers upon exposure to hyperoxia and that sex as a biological variable will modulate differences in expression. Wild-type (WT) and Cdh5-PAC CreERT2 (endothelial reporter) neonatal male and female mice (C57BL6) were exposed to hyperoxia (0.95 [Formula: see text]) either during the saccular stage of lung development (95% [Formula: see text];

Indexed as

Bronchopulmonary DysplasiaHyperoxiaLung InjuryAnimalsAnimals, NewbornEndothelial CellsFemaleHumansInfant, NewbornLungMaleMicebronchopulmonary dysplasiahuman pulmonary microvascular endothelial cellshyperoxianeonatalsex-specific

Identifiers

PMID37395632
PMCPMC10625841
OpenAlexW4382918511

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.