ArticleHeliyon2023
Overexpression of FSP1 Ameliorates ferroptosis via PI3K/ AKT /GSK3β pathway in PC12 cells with Oxygen-Glucose Deprivation/Reoxygenation.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- The SLC7A11 Thermostat: A Molecular Signaling Switch Between Ferroptosis and Disulfidptosis in Neurodegenerative Disease.Molecular neurobiology · 2026Review
- Article
- Metabolic alterations and redox homeostasis in ferroptosis: emerging mechanisms and therapeutic implications.Archives of medical science : AMS · 2026Article
- Inhibition of the P2Y2 Receptor Promotes Facial Nerve Function by Enhancing Neuron Autophagy.Current neuropharmacology · 2026Article
- Mollugin attenuates oxygen-glucose deprivation/reperfusion-induced brain microvascular endothelial cell death and permeability through activation of BDNF/TrkB-modulated Akt pathway.Journal of bioenergetics and biomembranes · 2025Article
- Perampanel Regulates Neuroinflammation and Ferroptosis via Activating FSP1 Following Brain Ischemia.Journal of inflammation research · 2025Article
- Six-methoxyflavone suppresses CircPIAS1 biogenesis via targeting PTBP1 and, in combination with IFN-γ, promotes ferroptosis in melanoma.Frontiers in pharmacology · 2025Article
- Edaravone Alleviates Traumatic Brain Injury by Inhibition of Ferroptosis via FSP1 Pathway.Molecular neurobiology · 2024Article
- Comprehensive cognition of yak (Animal biotechnology · 2024Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After ischemia and reperfusion (I/R), nerve cell damage is a pathogenic process that involves numerous molecular processes. In the last ten years, one new classification of programmed cell death is ferroptosis. More recent research has demonstrated that ferroptosis has a role in a variety of neurological disorders, including stroke, cancer, and neurodegenerative illnesses. Ferroptosis suppressor protein 1 (FSP1) plays a significant role in inhibiting ferroptosis. The purpose of this work is to determine how overexpression of FSP1 affects the ferroptosis of PC12 cells under the condition of oxygen-glucose deprivation/reoxygenation (OGD/R). The expression of FSP1 was regulated by lentivirus transfection technology. Western blot and immunofluorescence were used to measure protein levels related to ferroptosis and the PI3K/AKT/GSK3β signal pathway. Determine cell viability using the appropriate kit. Mitochondrial structural morphology was checked by transmission electron microscopy in PC12 cells. Reactive oxygen species (ROS) and Malondialdehyde (MDA) were quantified using the relevant kits. OGD/R induced ferroptosis in PC12 cells, however, FSP1 overexpression reverses ferroptosis and promotes cell viability, lowering ROS and MDA content. The expression of FSP1 decreased in OGD/R0h and OGD/R6h and rebounded in OGD/R24h and OGD/R48h. During the processes of OGD/R-induced ferroptosis, FSP1 overexpression significantly stimulated PI3K/AKT/GSK3β pathway, but LY294002 weakens the protective effect of FSP1 overexpression. Our outcomes demonstrate that overexpression of FSP1 markedly enhances the ability to resist ferroptosis via the PI3K/AKT/GSK3β pathway. The above results may provide a new preliminary lead for the treatment of the cerebral ischemia-reperfusion injury.
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