Evidence map›Paper›PMID 36046664›Full record

ArticleJournal of inflammation research2022

Vitamin D Ameliorates Apoptosis and Inflammation by Targeting the Mitochondrial and MEK1/2-ERK1/2 Pathways in Hyperoxia-Induced Bronchopulmonary Dysplasia.

Jinhui Hu, Zhixin Wu, Huawei Wang, Haifeng Geng, Jie Huo, Xueping Zhu, Xiaoli Zhu

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation research, 2022. 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
2.9field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. FTO-dependent mInflammation · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Observational
  12. Review
  13. Review
  14. Carbon dioxide and MAPK signalling: towards therapy for inflammation.Cell communication and signaling : CCS · 2023
    Review
  15. Molecular mechanisms of cell death in bronchopulmonary dysplasia.Apoptosis : an international journal on programmed cell death · 2023
    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

7 authors at 4 institutions in 1 country.

Jinhui Hu *Department of Neonatology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Zhixin Wu *Department of Neonatology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Huawei WangDepartment of Neonatology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Haifeng GengDepartment of Neonatology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Jie HuoDepartment of Neonatology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Xueping ZhuDepartment of Neonatology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Xiaoli ZhuDepartment of Intervention, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China.
Soochow University · CNFirst Affiliated Hospital of Soochow University · CNHangzhou Women’s Hospital · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Bronchopulmonary dysplasia (BPD) is a common and severe complication in preterm infants. Vitamin D (VitD) has been reported to protect against BPD; however, its role in the mitochondria-mediated and MEK1/2-ERK1/2 pathways has not yet been reported. Methods: We first performed in vivo studies using neonatal C57BL/6 mice in which we induced BPD by exposing them to a hyperoxic environment (85% O Results: The mean linear intercept, septal thickness, and abnormal fibrosis increased, while radial alveolar count decreased in BPD lungs compared to RA lungs. VitD administration was able to ameliorate the phenotype in BPD lungs. IL-6, IFN-γ, and TNF-α expression and the apoptotic rate decreased in the BPD+VitD lung group. VitD pretreatment restored abnormal mitochondrial morphology, reduced mitochondrial membrane loss, and reduced the expression of cleaved caspase-3, Bax, and Bcl-2 in BEAS-2B cells. VitD administration also reduced IL-6, IFN-γ, and TNF-α mRNA, as well as pMEK1/2 and pERK1/2 expression and apoptosis rate in cells exposed to hyperoxia. Conclusion: We concluded that VitD treatment ameliorated apoptosis and inflammation by targeting the mitochondrial pathway and via the MEK1/2-ERK1/2 signaling pathway in BPD, thus supporting its potential therapeutic use in this condition.

Indexed as

apoptosisbronchopulmonary dysplasiahyperoxiainflammationMEK1/2-ERK1/2mitochondriavitamin D

Identifiers

PMID36046664
PMCPMC9423049
OpenAlexW4293294938

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.