Evidence map›Paper›PMID 41296091›Full record

ReviewCellular and molecular neurobiology2025

Ferroptosis in Neonatal Hypoxic-Ischemic Encephalopathy: Mechanisms and the Therapeutic Potential of Vitamin D/VDR Signaling.

Yueju Cai, Wei Zhou

Abstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Vitamin DApplied microbiology and biotechnology · 2026
    Review
  3. Review
  4. 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

2 authors.

Yueju CaiDepartment of Neonatology, Guangzhou Wowen and Children's Medical Center, Guangzhou Medical University, No. 9 Jin Sui Road, Tianhe District, Guangzhou, 510623, China.ORCID http://orcid.org/0009-0009-3177-271X
Wei ZhouDepartment of Neonatology, Guangzhou Wowen and Children's Medical Center, Guangzhou Medical University, No. 9 Jin Sui Road, Tianhe District, Guangzhou, 510623, China. zhouwei_pu001@126.com.ORCID http://orcid.org/0009-0008-4893-1396

Funding

Liuzhou Science and Technology Planning Project 2024SB 0104A002Wu Jieping Medical Foundation Clinical Research Special Funding 320.6750.2025-9-15
6 · The paper itself

Abstract

As a major neonatal brain disorder, hypoxic-ischemic encephalopathy(HIE) presents with elevated risks of long-term disability and neonatal death. Ferroptosis is a distinct mode of regulated cell death marked by excess intracellular iron, oxidative lipid injury, and suppressed GPX4 activity, and has gained attention as a pivotal mechanism in the development of HIE. Signaling pathways such as Nrf2, TLR4/NF-κB, and endoplasmic reticulum stress(ERS) play critical roles.Vitamin D (VD) and its receptor (VDR), beyond their classical roles in calcium-phosphate homeostasis, as neuroprotective modulators of ferroptosis. VD/VDR signaling promotes antioxidant defenses (e.g., via the Nrf2/HO-1 pathway), restores GPX4 activity, regulates iron and lipid metabolism, and mitigates neuroinflammation.These insights provide a rationale for exploring VD/VDR-based interventions as adjunctive strategies to therapeutic hypothermia, which could potentially be explored to improve neurodevelopmental outcomes in affected neonates.

Indexed as

FerroptosisHypoxia-Ischemia, BrainReceptors, CalcitriolSignal TransductionVitamin DAnimalsHumansInfant, NewbornReceptors, CalcitriolVitamin DFerroptosisNeonatal hypoxic-ischemic encephalopathyNeuroprotectionVitamin DVitamin D receptor

Identifiers

PMID41296091
PMCPMC12657705

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.