ArticleCell death & disease2022
Ferroptosis in oligodendrocyte progenitor cells mediates white matter injury after hemorrhagic stroke.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 71 citations in OpenAlex.
- Irisin Restrains Oligodendroglial Ferroptosis to Preserve White Matter After Traumatic Brain Injury via AMPK Activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Spatiotemporal profiling of white matter lesions and their contribution in the pathologies of Parkinson's disease animal models.GeroScience · 2026Article
- White matter injury in neonatal rats is attenuated by GsMTx4 inhibiting oligodendrocyte precursor cell ferroptosis via the PIEZO1/GCLC signaling pathway.Pediatric research · 2026Article
- Nanomedicines and stroke: Advantages in chronic inflammation treatment and neural regeneration.Neural regeneration research · 2026Article
- Enhancing exosomes efficacy with engineered nanozymes for a multi-targeted combination strategy in osteoarthritis treatment.Materials today. Bio · 2026Article
- Stage-specific CHI3L1/YKL-40 signaling controls generation of oligodendrocyte precursor cells through IL13Rα2-mediated ferroptosis.bioRxiv : the preprint server for biology · 2026Article
- Deferoxamine mitigates neuronal loss following spinal cord injury via ferroptosis inhibition and Nrf2/HO‑1 pathway activation.International journal of molecular medicine · 2026Article
- When Pathways Converge: Iron, Lipid Peroxidation, and α-Synuclein in Ferroptosis-Driven Dopaminergic Neurodegeneration.Journal of neurochemistry · 2026Review
- Review
- Neurovascular Unit-Derived Extracellular Vesicles as Regulators of Post-Stroke Pathology and Neurorestoration.Biomolecules · 2026Review
- Oligodendrocyte: Development, Plasticity, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Metabolic Regulatory Networks in Ferroptosis During Alzheimer's Disease, Mechanisms of Glial Cell Action, and Pathological Correlations with Neuritic Plaques.International journal of general medicine · 2026Review
- Aberrant adenosine ANature communications · 2025Article
- Zmiz1-Mediated SUMOylation of NLRP3 Inflammasome Regulates Satellite Glial Cell Activation and Neuronal Autophagy in Trigeminal Neuralgia.Inflammation · 2025Article
- Neonatal sevoflurane exposures inhibits DHHC5-mediated palmitoylation of TfR1 in oligodendrocytes, leading to hypomyelination and neurological impairments.Journal of advanced research · 2025Article
- Ferroptosis in Human Diseases: Fundamental Roles and Emerging Therapeutic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Metabolic reprogramming in ischemic stroke: when glycolytic overdrive meets lipid storm.Cell death & disease · 2025Review
- Single-nucleus transcriptomic profiling reveals temporal dynamics of neuroinflammation and myelin repair after intracerebral haemorrhage.Clinical and translational medicine · 2025Article
- Iron and selenium: At the crossroads of development and death in oligodendrocytes.Archives of biochemistry and biophysics · 2025Review
- Neuroferroptosis in health and diseases.Nature reviews. Neuroscience · 2025Review
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oligodendrocyte progenitor cells (OPCs) differentiate to myelin-producing mature oligodendrocytes and enwrap growing or demyelinated axons during development and post central nervous diseases. Failure of remyelination owing to cell death or undifferentiation of OPCs contributes to severe neurologic deficits and motor dysfunction. However, how to prevent the cell death of OPCs is still poorly understood, especially in hemorrhagic diseases. In the current study, we injected autologous blood into the mouse lateral ventricular to study the hemorrhage-induced OPC cell death in vivo. The integrity of the myelin sheath of the corpus callosum was disrupted post intraventricular hemorrhage (IVH) assessed by using magnetic resonance imaging, immunostaining, and transmission electron microscopy. Consistent with the severe demethylation, we observed massive cell death of oligodendrocyte lineages in the periventricular area. In addition, we found that ferroptosis is the major cell death form in Hemin-induced OPC death by using RNA-seq analysis, and the mechanism was glutathione peroxidase 4 activity reduction-resulted lipid peroxide accumulation. Furthermore, inhibition of ferroptosis rescued OPC cell death in vitro, and in vivo attenuated IVH-induced white matter injury and promoted recovery of neurological function. These data demonstrate that ferroptosis is an essential form of OPC cell death in hemorrhagic stroke, and rescuing ferroptotic OPCs could serve as a therapeutic target for stroke and related diseases.
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Registered trials
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