ArticleCNS neuroscience & therapeutics2024
DMT1 ubiquitination by Nedd4 protects against ferroptosis after intracerebral hemorrhage.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 18 citations in OpenAlex.
- Lysosomes in Ferroptosis: Regulatory Mechanisms and Molecular Targets.Molecules (Basel, Switzerland) · 2026Review
- Biomaterial-based strategies targeting ferroptosis for alleviating intervertebral disc degeneration: Advances and perspectives.Journal of orthopaedic translation · 2026Review
- Organelle regulation of ferroptosis after intracerebral hemorrhage.Redox biology · 2026Review
- Curcumin Protects Mouse Spermatogonia from Triptolide-Induced Injury Through Modulation of Ferroptosis-Related Pathways.Biology · 2026Article
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- Ferroptosis in Cerebral Ischemia/Reperfusion Injury: Mechanistic Drivers and Therapeutic Frontiers.Neuropsychiatric disease and treatment · 2026Review
- NEDD4 promotes reactive astrogliosis by enhancing K63-linked ubiquitination and inhibiting chaperone-mediated autophagy degradation of YAP1.International journal of biological sciences · 2026Article
- Osteoarthritis pathogenesis Unveiled: DMT1 drives autophagy-dependent ferroptosis through a mir-17-5p/NEDD4 regulatory axis.Journal of orthopaedic translation · 2026Article
- NEDD4 suppresses ferroptosis in lung ischemia-reperfusion injury by ubiquitinating and degrading SLC1A5.Scientific reports · 2025Article
- The Roles of E3 Ubiquitin Ligases in Cerebral Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
- MK5 Regulates Microglial Activation and Neuroinflammation in Experimental Stroke Models.CNS neuroscience & therapeutics · 2025Article
- Tungsten-based polyoxometalate nanoclusters as ferroptosis inhibitors modulating S100A8/A9-mediated iron metabolism pathway for managing intracerebral haemorrhage.Journal of nanobiotechnology · 2025Article
- Identification and validation of diagnostic biomarkers for temporal lobe epilepsy related to ferroptosis and potential therapeutic targets.Scientific reports · 2025Article
- Ferroptosis-associated pathological injury mechanisms and therapeutic strategies after intracerebral hemorrhage.Frontiers in neurology · 2025Review
- Targeting ferroptosis with natural products in stroke: therapeutic mechanisms and translational opportunities.Frontiers in pharmacology · 2025Review
- DMT1 ubiquitination by Nedd4 protects against ferroptosis after intracerebral hemorrhage.CNS neuroscience & therapeutics · 2024Article
- The critical role of MLKL in hemorrhagic stroke and the therapeutic potential of its associated protein network.Frontiers in cell and developmental biology · 2024Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveNeuronal precursor cells expressed developmentally down-regulated 4 (Nedd4) are believed to play a critical role in promoting the degradation of substrate proteins and are involved in numerous biological processes. However, the role of Nedd4 in intracerebral hemorrhage (ICH) remains unknown. This study aims to investigate the regulatory role of Nedd4 in the ICH model.
methodsMale C57BL/6J mice were induced with ICH. Subsequently, the levels of glutathione peroxidase 4 (GPX4), malondialdehyde (MDA) concentration, iron content, mitochondrial morphology, as well as the expression of divalent metal transporter 1 (DMT1) and Nedd4 were assessed after ICH. Furthermore, the impact of Nedd4 overexpression was evaluated through analyses of hematoma area, ferroptosis, and neurobehavioral function. The mechanism underlying Nedd4-mediated degradation of DMT1 was elecidated using immunoprecipitation (IP) after ICH.
resultsUpon ICH, the level of DMT1 in the brain increased, but decreased when Nedd4 was overexpressed using Lentivirus, suggesting a negative correlation between Nedd4 and DMT1. Additionally, the degradation of DMT1 was inhibited after ICH. Furthermore, it was found that Nedd4 can interact with and ubiquitinate DMT1 at lysine residues 6, 69, and 277, facilitating the degradation of DMT1. Functional analysis indicated that overexpression of Nedd4 can alleviate ferroptosis and promote recovery following ICH.
conclusionThe results demonstrated that ferroptosis occurs via the Nedd4/DMT1 pathway during ICH, suggesting it potential as a valuable target to inhibit ferroptosis for the treatment of ICH.
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