ArticleCNS neuroscience & therapeutics2024
KA-mediated excitotoxicity induces neuronal ferroptosis through activation of ferritinophagy.
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 7 papers.
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Who cites it
7 citing papers in PubMed.
- Poly-GR promotes ferroptosis-associated vulnerability in C9orf72-ALS.Cell & bioscience · 2026Article
- Notch-1 suppressed vascular dementia via modulating AMPK/mTOR/TFEB/YAP signaling induced ferroptosis.European journal of medical research · 2026Article
- Molecular mechanisms of excitotoxicity and their relevance to the pathogenesis of neurodegenerative diseases-an update.Acta pharmacologica Sinica · 2025Review
- Fluvoxamine Attenuates Blood-Brain Barrier Disruption in Drug-Resistance Epilepsy and inhibits Ferroptosis via the Sigma-1 Receptor-TAMM41 signaling in bEnd.3 cells.Molecular neurobiology · 2025Article
- Emerging Therapeutic Strategies in Intracerebral Hemorrhage: Enhancing Neurogenesis and Functional Recovery.MedComm · 2025Review
- The Role of Autophagy in Excitotoxicity, Synaptic Mitochondrial Stress and Neurodegeneration.Autophagy reports · 2025Article
- KA-mediated excitotoxicity induces neuronal ferroptosis through activation of ferritinophagy.CNS neuroscience & therapeutics · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
objectivesThis study aims to elucidate the role of Fe
methodsWestern blotting was used to detect the expression of FTH1, NCOA4, Lamp2, TfR, FPN, and DMT1 after KA stereotaxic injection into the unilateral striatum of mice. Colocalization of Fe
resultsWestern blot results showed that the expression of NCOA4, DMT1, and Lamp2 was significantly upregulated, while FTH1 was downregulated, but there were no significant changes in TfR and FPN. The fluorescence results indicated that KA enhanced the colocalization of free Fe
conclusionKA-induced excitotoxicity activates ferritinophagy, and targeting ferritinophagy effectively inhibits downstream ferroptosis. Interference with NCOA4 effectively attenuates KA-induced neuronal damage. This study provides a potential therapeutic target for excitotoxicity related disease conditions.
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Registered trials
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