Evidence map›Paper›PMID 39102510›Full record

ArticleRedox report : communications in free radical research2024

Hyperoxia exposure induces ferroptosis and apoptosis by downregulating PLAGL2 and repressing HIF-1α/VEGF signaling pathway in newborn alveolar typeII epithelial cell.

Yuting Zhu, Hongmei Hou, Yawen Li, Yanyu Zhang, Yuanyuan Fang, Si Chen, Le Zhang, Weilai Jin, Yahui Zhou

Abstract read
In one paragraph

Article in Redox report : communications in free radical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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  14. Mechanisms ofIntegrative cancer therapies
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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

9 authors.

Yuting ZhuDepartment of Neonatology, The Affiliated Children's Hospital of Jiangnan University, Wuxi, People's Republic of China.
Hongmei HouDepartment of Neonatology, The Affiliated Children's Hospital of Jiangnan University, Wuxi, People's Republic of China.
Yawen LiDepartment of Neonatology, The Affiliated Children's Hospital of Jiangnan University, Wuxi, People's Republic of China.
Yanyu ZhangDepartment of Neonatology, The Affiliated Children's Hospital of Jiangnan University, Wuxi, People's Republic of China.
Yuanyuan FangDepartment of Neonatology, The Affiliated Children's Hospital of Jiangnan University, Wuxi, People's Republic of China.
Si ChenDepartment of Neonatology, The Affiliated Children's Hospital of Jiangnan University, Wuxi, People's Republic of China.
Le ZhangDepartment of Neonatology, The Affiliated Children's Hospital of Jiangnan University, Wuxi, People's Republic of China.
Weilai JinDepartment of Neonatology, The Affiliated Children's Hospital of Jiangnan University, Wuxi, People's Republic of China.
Yahui ZhouDepartment of Neonatology, The Affiliated Children's Hospital of Jiangnan University, Wuxi, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroudBronchopulmonary dysplasia (BPD) is one of the most important complications plaguing neonates and can lead to a variety of sequelae. the ability of the HIF-1α/VEGF signaling pathway to promote angiogenesis has an important role in neonatal lung development.

methodNewborn rats were exposed to 85% oxygen. The effects of hyperoxia exposure on Pleomorphic Adenoma Gene like-2 (PLAGL2) and the HIF-1α/VEGF pathway in rats lung tissue were assessed through immunofluorescence and Western Blot analysis. In cell experiments, PLAGL2 was upregulated, and the effects of hyperoxia and PLAGL2 on cell viability were evaluated using scratch assays, CCK-8 assays, and EDU staining. The role of upregulated PLAGL2 in the HIF-1α/VEGF pathway was determined by Western Blot and RT-PCR. Apoptosis and ferroptosis effects were determined through flow cytometry and viability assays.

resultsCompared with the control group, the expression levels of PLAGL2, HIF-1α, VEGF, and SPC in lung tissues after 3, 7, and 14 days of hyperoxia exposure were all decreased. Furthermore, hyperoxia also inhibited the proliferation and motility of type II alveolar epithelial cells (AECII) and induced apoptosis in AECII. Upregulation of PLAGL2 restored the proliferation and motility of AECII and suppressed cell apoptosis and ferroptosis, while the HIF-1α/VEGF signaling pathway was also revived.

conclusionsWe confirmed the positive role of PLAGL2 and HIF-1α/VEGF signaling pathway in promoting BPD in hyperoxia conditions, and provided a promising therapeutic targets.

Indexed as

Alveolar Epithelial CellsAnimals, NewbornApoptosisFerroptosisHyperoxiaHypoxia-Inducible Factor 1, alpha SubunitSignal TransductionVascular Endothelial Growth Factor AAnimalsCell ProliferationDown-RegulationHumansRatsRats, Sprague-DawleyTranscription FactorsHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitTranscription FactorsVascular Endothelial Growth Factor Avascular endothelial growth factor A, ratBronchopulmonary dysplasia (BPD)HIF-1α/VEGF pathwaylung injuryPLAGL 2

Identifiers

PMID39102510
PMCPMC11302460

What Socratic holds

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Registered trials

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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 Socratic graph.