ArticleCNS neuroscience & therapeutics2024
MEF2C Alleviates Postoperative Cognitive Dysfunction by Repressing Ferroptosis.
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 13 papers.
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Who cites it
13 citing papers in PubMed.
- Dexmedetomidine inhibits microglia ferroptosis to relieve postoperative cognitive dysfunction in elderly rats through JPX/HIF-1/DHODH pathway.Experimental brain research · 2026Article
- Targeting Ferroptosis Pathways for Synaptic Protection in Sevoflurane-Induced Cognitive Impairment: A Nanomedicine Approach.CNS neuroscience & therapeutics · 2026Review
- c-MAF Transcriptionally Activates Slc40a1 to Repress Ferroptosis in Sepsis-Associated Encephalopathy.CNS neuroscience & therapeutics · 2026Article
- Plasma-Derived Exosomal hsa-miR-3677-3p Induces Ferroptosis in Neurons by Targeting ABCB8 in Perioperative Neurocognitive Disorders After Prostate Surgery.Neurochemical research · 2026Article
- Morin improves postoperative cognitive dysfunction by mediating the miR-138-5p/SIRT1 axis to regulate ferroptosis.Scientific reports · 2026Article
- Ferroptosis: an emerging key mechanism linking aging, surgical and anesthetic exposure to postoperative cognitive dysfunction.Frontiers in immunology · 2026Review
- Comprehensive analysis of circRNA-miRNA-mRNA networks to reveal potential cell death, inflammation and oxidative stress-related targets for postoperative cognitive dysfunction.Frontiers in aging neuroscience · 2026Article
- Electroacupuncture Pretreatment Ameliorates Perioperative Neurocognitive Disorder in Aged Mice by Inhibiting Ferroptosis Through the SIRT1/NRF2/GPX4 Pathway.Journal of cellular and molecular medicine · 2026Article
- Decoding neuroimmune ferroptotic vulnerability in isoflurane-induced neonatal neurotoxicity via the SLC7A11/GPX4 axis.Frontiers in pharmacology · 2026Article
- Microglial RUNX1/RBM47 ablation inhibits neuronal ferroptosis via regulating the cGAS-STING-MEF2C pathway in mice with postoperative cognitive dysfunction.Communications biology · 2025Article
- Sirtuin-3 activation by honokiol attenuated anesthesia/surgery-induced cognitive impairment and neuronal ferroptosis via inhibiting mitochondrial GPX4 acetylation.Journal of nanobiotechnology · 2025Article
- Transcriptome Insights into Protective Mechanisms of Ferroptosis Inhibition in Aortic Dissection.International journal of molecular sciences · 2025Article
- Anesthesia-Induced Ferroptosis: Bidirectional Regulation and Molecular Mechanisms in Cardio-Cerebral Injury.Journal of inflammation research · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundFerroptosis, a form of programmed cell death featured by lipid peroxidation, has been proposed as a potential etiology for postoperative cognitive dysfunction (POCD). Myocyte-specific enhancer factor 2C (MEF2C), a transcription factor expressed in various brain cell types, has been implicated in cognitive disorders. This study sought to ascertain whether MEF2C governs postoperative cognitive capacity by affecting ferroptosis.
methodsTranscriptomic analysis of public data was used to identify MEF2C as a candidate differentially expressed gene in the hippocampus of POCD mice. The POCD mouse model was established via aseptic laparotomy under isoflurane anesthesia after treatment with recombinant adeno-associated virus 9 (AAV9)-mediated overexpression of MEF2C and/or the glutathione peroxidase 4 (GPX4) inhibitor RSL3. Cognitive performance, Nissl staining, and ferroptosis-related parameters were assessed. Dual-luciferase reporter gene assays and chromatin immunoprecipitation assays were implemented to elucidate the mechanism by which MEF2C transcriptionally activates GPX4.
resultsMEF2C mRNA and protein levels decreased in the mouse hippocampus following anesthesia and surgery. MEF2C overexpression ameliorated postoperative memory decline, hindered lipid peroxidation and iron accumulation, and enhanced antioxidant capacity, which were reversed by RSL3. Additionally, MEF2C was found to directly bind to the Gpx4 promoter and activate its transcription.
conclusionsOur findings suggest that MEF2C may be a promising therapeutic target for POCD through its negative modulation of ferroptosis.
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