ArticleCellular and molecular neurobiology2019
Inhibition of VDAC1 Protects Against Glutamate-Induced Oxytosis and Mitochondrial Fragmentation in Hippocampal HT22 Cells.
Article in Cellular and molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 59 citations in OpenAlex.
- The fruitfly Drosophila melanogaster as an in vivo model of ferroptosis.Redox biology · 2026Article
- GHRHR Deficiency Enhances Retinal Ganglion Cell Survival and Visual Functions in Experimental Glaucoma by Inhibiting Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Research progress of ferroptosis in obesity and its complications.Journal of physiology and biochemistry · 2026Review
- Signaling pathways regulating VDAC1 overexpression associated with apoptosis, pyroptosis, and ferroptosis.Cell communication and signaling : CCS · 2026Article
- NDUFA4 Deletion Upregulates VDAC1 to Promote Mitochondrial Damage, Endoplasmic Reticulum Expansion, and Neuronal Apoptosis.Human mutation · 2026Article
- SAT1 Knockdown Decreases Glutamate-Induced Oxidative Stress, Ferroptosis, and Apoptosis in HT22 Cells via Activating the Nrf2/ARE Pathway.Neuromolecular medicine · 2025Article
- Ferroptosis: a new target for depression prevention and treatment.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Resveratrol Inhibits VDAC1-Mediated Mitochondrial Dysfunction to Mitigate Pathological Progression in Parkinson's Disease Model.Molecular neurobiology · 2025Article
- The metabolites of gut microbiota: their role in ferroptosis in inflammatory bowel disease.European journal of medical research · 2025Review
- Modulation of mitochondrial voltage dependent anion channel: studies on bilayer electrophysiology.Frontiers in physiology · 2025Review
- Excitotoxicity, Oxytosis/Ferroptosis, and Neurodegeneration: Emerging Insights into Mitochondrial Mechanisms.Aging and disease · 2024Review
- A critical appraisal of ferroptosis in Alzheimer's and Parkinson's disease: new insights into emerging mechanisms and therapeutic targets.Frontiers in pharmacology · 2024Review
- Inhibition of Oxidative Stress-Induced Ferroptosis Can Alleviate Rheumatoid Arthritis in Human.Journal of immunology research · 2024Article
- Mapping the Research of Ferroptosis in Parkinson's Disease from 2013 to 2023: A Scientometric Review.Drug design, development and therapy · 2024Review
- Tanshinone IIA confers protection against myocardial ischemia/reperfusion injury by inhibiting ferroptosis and apoptosis via VDAC1.International journal of molecular medicine · 2023Article
- MIRO-1 interacts with VDAC-1 to regulate mitochondrial membrane potential in Caenorhabditis elegans.EMBO reports · 2023Article
- Inhibition of extranodal NK/T-cell lymphoma by Chiauranib through an AIF-dependent pathway and its synergy with L-asparaginase.Cell death & disease · 2023Article
- Impact of Calcium Influx on Endoplasmic Reticulum in Excitotoxic Neurons: Role of Chemical Chaperone 4-PBA.Cellular and molecular neurobiology · 2023Article
- The E3 ubiquitin ligase NEDD4-1 protects against acetaminophen-induced liver injury by targeting VDAC1 for degradation.Acta pharmaceutica Sinica. B · 2023Article
- Inhibition of VDAC1 Rescues AMediators of inflammation · 2023Article
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4 authors at 1 institution in 1 country.
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Abstract
The involvement of glutamate in neuronal cell death in neurodegenerative diseases and neurotrauma is mediated through excitotoxicity or oxytosis. The latter process induces oxidative stress via glutamate-mediated inhibition of cysteine transporter xCT, leading to depletion of the cellular glutathione pool. Mitochondrial damage, loss of mitochondrial membrane potential (MMP), and depletion of energy metabolites have been shown in this process. The Voltage-Dependent Anion Channel-1 (VDAC1) is one of the main components of the mitochondrial outer membrane and plays a gatekeeping role in mitochondria-cytoplasm transport of metabolites. In this study, we explored the possible participation of VDAC-1 in the pathophysiology of oxytosis. Administration of glutamate in HT22 cells that lack the glutamate ionotropic receptors induced an upregulation and oligomerization of VDAC1. This was associated with an increase in ROS and loss of cell survival. Glutamate-mediated oxytosis in this model also decreased MMP and promoted ATP depletion, resulting in translocation of cytochrome c (cyt C) and apoptosis inducing factor (AIF) from mitochondria into the cytosol. This was also accompanied by cleavage of AIF to form truncated AIF. Inhibition of VDAC1 oligomerization using 4,4'-Diisothiocyanatostilbene-2,2'-disulfonate (DIDS), significantly improved the cell survival, decreased the ROS levels, improved mitochondrial functions, and decreased the mitochondrial damage. Notably, DIDS also inhibited the mitochondrial fragmentation caused by glutamate, indicating the active role of VDAC1 oligomerization in the process of mitochondrial fragmentation in oxytosis. These results suggest a critical role for VDAC1 in mitochondrial fragmentation and its potential therapeutic value against glutamate-mediated oxidative neurotoxicity.
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