ArticleTranslational pediatrics2022
Vitamin D suppresses ferroptosis and protects against neonatal hypoxic-ischemic encephalopathy by activating the Nrf2/HO-1 pathway.
Article in Translational pediatrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Hypoxic-Ischemic Encephalopathy: Pathogenesis and Promising Therapies.Molecular neurobiology · 2025Pooled it
- The interplay between vitamin D3 and Nrf2 signaling: mechanistic insights and therapeutic potentials.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Dietary Intake of 25-Hydroxy Vitamin D3 from First Feeding Improves Feed Efficiency and Modulates Hepatic Metabolic Transcriptome in Rainbow Trout.Marine biotechnology (New York, N.Y.) · 2026Article
- Combined Vitamin D and Resveratrol Treatment Attenuates Motor Deficits and Neurodegeneration in a 6-OHDA Mouse Model of Parkinson's Disease in Male Mice: A Focus on Sirt1 and Lingo-1 Pathways in the Ventral Tegmental Area.Brain and behavior · 2026Article
- Vitamin D Promotes Neuronal Survival via Nrf2 Upregulation in D-Galactose-Induced Mice: An In-Vivo and In-Silico Study.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Association of vitamin D with sepsis incidence and mortality: a large population-based prospective cohort study.Critical care (London, England) · 2026Article
- Whole-body vs. selective head cooling and target temperature strategies for neonatal HIE: a meta-analysis of long-term outcomes.Frontiers in pediatrics · 2026Review
- Ferroptosis in Neonatal Hypoxic-Ischemic Encephalopathy: Mechanisms and the Therapeutic Potential of Vitamin D/VDR Signaling.Cellular and molecular neurobiology · 2025Review
- Article
- The Role of Vitamin D and Vitamin D Receptor in Sepsis.Current issues in molecular biology · 2025Review
- Targeting LINC00707 by vitamin D3 attenuates nitrogen mustard-caused dermal toxicity through inhibiting ferroptosis.Redox biology · 2025Article
- Vitamin D ameliorates prediabetic cardiac injure via modulation of the ErbB4/ferroptosis signaling axis.Frontiers in immunology · 2025Article
- Evaluating the Prophylactic and Nephroprotective Effects of Vitamin D and Metformin in Diabetic Nephropathy.Oxidative medicine and cellular longevity · 2025Article
- Harnessing the gut microbiome to modulate ferroptosis: a metabolic strategy for the treatment of digestive tract cancers.Frontiers in immunology · 2025Review
- 25-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese Chickens.Antioxidants (Basel, Switzerland) · 2024Article
- Enhancing 7-dehydrocholesterol suppresses brain ferroptosis and tissue injury after neonatal hypoxia-ischemia.Scientific reports · 2024Article
- A ferroptosis-related ceRNA network for investigating the molecular mechanisms and the treatment of neonatal hypoxic-ischemic encephalopathy.Translational pediatrics · 2024Article
- The biphasic role of Hspb1 on ferroptotic cell death in Parkinson's disease.Theranostics · 2024Article
- Is oxidative stress - antioxidants imbalance the physiopathogenic core in pediatric obesity?Frontiers in immunology · 2024Review
- Ferrostatin-1 attenuates hypoxic-ischemic brain damage in neonatal rats by inhibiting ferroptosis.Translational pediatrics · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Hypoxic-ischemic encephalopathy (HIE) is a major cause of neonatal death, and vitamin D (VD) is a neuroprotection nutrition whose deficiency is associated with its risk. However, the mechanism of VD involved in neonatal HIE is not well known. Methods: In this experiment a hypoxic-ischemic brain damage (HIBD) model was established by using the Rice-Vannucci method, rats were intraperitoneally injected with 0.1 µg/kg VD every day for two weeks. The brain damage and mitochondria injury were examined by hematoxylin-eosin (HE) staining and transmission electron microscope (TEM), respectively. The oxidation response and inflammatory factors were determined by enzyme-linked immunosorbent assay (ELISA), and the cell viability was determined by Cell Counting Kit-8 (CCK-8). mRNA and protein expression were detected by quantitative real real-time PCR (qRT-PCR), Western blot, and immunofluorescence. Results: The results showed VD effectively ameliorated brain histologic damage and mitochondria injury induced by hypoxic ischemia (HI). VD elevated the expression of Nrf2 and HO-1, which resulted in increased levels of GPX4, superoxide dismutase (SOD), and glutathione (GSH) and reduced content of malondialdehyde (MDA) and reactive oxygen species (ROS), resulting in decreased ferroptosis in HI-treated rats. Moreover, VD reduced the secretion of inflammatory factors, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β. Conclusions: VD suppresses ferroptosis through activation of the Nrf2/HO-1 signaling pathway and exerts a protective role in neonatal HIE.
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