ArticleNeurochemical research2022
Ferritinophagy is Involved in Experimental Subarachnoid Hemorrhage-Induced Neuronal Ferroptosis.
Article in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Ferroptosis as a Form of Cell Death-Medical Importance and Pharmacological Implications.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Iron Hemostasis in Patients With Subarachnoid Hemorrhage and the Role of Early CSF Drainage.Neurology · 2025Review
- The intersection of ferroptosis and non-coding RNAs: a novel approach to ovarian cancer.European journal of medical research · 2025Review
- Natural flavonoids from herbs and nutraceuticals as ferroptosis inhibitors in central nervous system diseases: current preclinical evidence and future perspectives.Frontiers in pharmacology · 2025Review
- Ferroptosis in central nervous system injuries: molecular mechanisms, diagnostic approaches, and therapeutic strategies.Frontiers in cellular neuroscience · 2025Review
- Iron Metabolism and Ferroptosis in Early Brain Injury after Subarachnoid Haemorrhage.Molecular neurobiology · 2024Review
- Regulating NCOA4-Mediated Ferritinophagy for Therapeutic Intervention in Cerebral Ischemia-Reperfusion Injury.Neurochemical research · 2024Article
- Melatonin alleviates septic ARDS by inhibiting NCOA4-mediated ferritinophagy in alveolar macrophages.Cell death discovery · 2024Article
- Rasd1 is involved in white matter injury through neuron-oligodendrocyte communication after subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2024Article
- Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature.Chinese neurosurgical journal · 2024Review
- Deferoxamine Mitigates Ferroptosis and Inflammation in Hippocampal Neurons After Subarachnoid Hemorrhage by Activating the Nrf2/TXNRD1 Axis.Molecular neurobiology · 2024Article
- Hypoxia Aggravates Neuron Ferroptosis in Early Brain Injury Following Subarachnoid Hemorrhage via NCOA4-Meditated Ferritinophagy.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- The mechanism of ferroptosis in early brain injury after subarachnoid hemorrhage.Frontiers in immunology · 2023Review
- The Regulated Cell Death and Potential Interventions in Preterm Infants after Intracerebral Hemorrhage.Current neuropharmacology · 2023Review
- The role of autophagy and apoptosis in early brain injury after subarachnoid hemorrhage: an updated review.Molecular biology reports · 2022Review
- Scrutinizing the Therapeutic Promise of Purinergic Receptors Targeting Depression.Neurotoxicity research · 2022Review
- Tetrandrine Ameliorates Traumatic Brain Injury by Regulating Autophagy to Reduce Ferroptosis.Neurochemical research · 2022Article
- Aquaporin 4 Depolarization-Enhanced Transferrin Infiltration Leads to Neuronal Ferroptosis after Subarachnoid Hemorrhage in Mice.Oxidative medicine and cellular longevity · 2022Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Ferroptosis is a novel form of regulated cell death involved in the pathophysiological process of experimental subarachnoid hemorrhage (SAH), but how neuronal ferroptosis occurs remains unknown. In this study, we report that SAH-induced ferroptosis is macroautophagy/autophagy dependent because the inhibition of autophagy by knocking out autophagy-related gene 5 (ATG5) apparently mitigated SAH-induced ferroptosis. We created an experimental SAH model in Sprague-Dawley rats to determine the possible mechanism. We found that SAH can trigger neuronal ferroptosis, as evidenced by the disruption of iron homeostasis, elevation of intracellular lipid peroxidation (LPO) and decreased expression of ferroptosis-protective proteins. Then, we inhibited autophagy by ATG5 gene knockout, showing that autophagy inhibition can reduce the intracellular iron level and LPO, improve the expression of ferroptosis-protective proteins, and subsequently alleviate SAH-induced cell death. Additionally, autophagy inhibition also attenuated SAH prognostic indicators, such as brain edema, blood-brain barrier permeability, and neurological deficits. These findings not only present an opinion that SAH triggers neuronal ferroptosis via activation of ferritinophagy but also indicate that regulating ferritinophagy and maintaining iron homeostasis could provide clues for the prevention of early brain injury.
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