ArticleCNS neuroscience & therapeutics2024
Fat mass and obesity associated protein inhibits neuronal ferroptosis via the FYN/Drp1 axis and alleviate cerebral ischemia/reperfusion injury.
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 23 papers.
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Who cites it
23 citing papers in PubMed, 24 citations in OpenAlex.
- Mitochondrial Fusion and Fission in Age-Related Cardio-Cerebral Diseases: Mechanisms and Interventions.Aging cell · 2026Review
- Mitochondrial dysfunction‑driven ferroptosis in cerebral ischemia‑reperfusion injury: Mechanisms and therapeutic strategies (Review).Molecular medicine reports · 2026Review
- N6-Methyladenosine Demethylase FTO Mitigates Cerebral Ischemia-Reperfusion Injury by Suppressing AQP4 Expression.CNS neuroscience & therapeutics · 2026Article
- Biphasic oxygen-regulating cyanobacterial hydrogel for synergistic ischemic stroke gas therapy and post-stroke depression prevention.Materials today. Bio · 2026Article
- N 6 -methyladenosine modification regulates cell death in cognitive impairment.Neural regeneration research · 2026Article
- Association of Weight-Adjusted-Waist Index With Brain Health: A 16-Year Population-Based Longitudinal Cohort Study.CNS neuroscience & therapeutics · 2026Article
- The Role of NMedComm · 2026Review
- Inhibiting the Hif-1α-Drp1 axis alleviates mitochondrial dysfunction and reduces senescence-like changes in myocardial tissue after acute myocardial infarction.Biology direct · 2026Article
- The Role of Cold-Inducible RNA-Binding Protein (CIRP) in Neurological Disorders.Brain sciences · 2026Review
- Regulation of FTO on PDCD5 mRNA stability to mediate neuron apoptosis in rats with hypoxic-ischemic brain damage.Translational neuroscience · 2026Article
- FTO-Mediated Mitigation of Ferroptosis Occurs in an ACSL4-Dependent Manner in Diabetic Cardiomyopathy.Cardiovascular toxicology · 2025Article
- Cold-Induced RNA-Binding Protein (CIRP) Affects Cerebral Ischemia-Reperfusion Injury Through NF-κB Pathway.Molecular neurobiology · 2025Article
- Targeting Drp1 in Cerebral Ischemia-Reperfusion Injury: Mechanisms and Therapeutic Implications.CNS neuroscience & therapeutics · 2025Review
- Mitochondrial Quality Control in Health and Disease.MedComm · 2025Review
- Elevated Plasma m6A Demethylase FTO Levels Predict Favorable Outcomes Following Acute Ischemic Stroke.Cellular and molecular neurobiology · 2025Article
- Safflower Yellow Pigment Alleviates Cerebral Ischemia-Reperfusion Injury via Protein Nitration and Oxidative Modulation.Brain and behavior · 2025Article
- Ferroptosis triggers mitochondrial fragmentation via Drp1 activation.Cell death & disease · 2025Article
- Insights into targeted ferroptosis in mechanisms, biology, and role of Alzheimer's disease: an update.Frontiers in aging neuroscience · 2025Review
- PANoptosis in neurological disorders: mechanisms, implications, and therapeutic potential.Frontiers in immunology · 2025Review
- The melatonin-FTO-ATF4 signaling pathway protects granulosa cells from cisplatin-induced chemotherapeutic toxicity by suppressing ferroptosis.Journal of assisted reproduction and genetics · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesFTO is known to be involved in cerebral ischemia/reperfusion (I/R) injury. However, its related specific mechanisms during this condition warrant further investigations. This study aimed at exploring the impacts of FTO and the FYN/DRP1 axis on mitochondrial fission, oxidative stress (OS), and ferroptosis in cerebral I/R injury and the underlying mechanisms.
methodsThe cerebral I/R models were established in mice via the temporary middle cerebral artery occlusion/reperfusion (tMCAO/R) and hypoxia/reoxygenation models were induced in mouse hippocampal neurons via oxygen-glucose deprivation/reoxygenation (OGD/R). After the gain- and loss-of-function assays, related gene expression was detected, along with the examination of mitochondrial fission, OS- and ferroptosis-related marker levels, neuronal degeneration and cerebral infarction, and cell viability and apoptosis. The binding of FTO to FYN, m6A modification levels of FYN, and the interaction between FYN and Drp1 were evaluated.
resultsFTO was downregulated and FYN was upregulated in tMCAO/R mouse models and OGD/R cell models. FTO overexpression inhibited mitochondrial fission, OS, and ferroptosis to suppress cerebral I/R injury in mice, which was reversed by further overexpressing FYN. FTO overexpression also suppressed mitochondrial fission and ferroptosis to increase cell survival and inhibit cell apoptosis in OGD/R cell models, which was aggravated by additionally inhibiting DRP1. FTO overexpression inhibited FYN expression via the m6A modification to inactive Drp1 signaling, thus reducing mitochondrial fission and ferroptosis and enhancing cell viability in cells.
conclusionsFTO overexpression suppressed FYN expression through m6A modification, thereby subduing Drp1 activity and relieving cerebral I/R injury.
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