ArticleAnnals of neurology2023
Selective Neuronal Knockout of STAT3 Function Inhibits Epilepsy Progression, Improves Cognition, and Restores Dysregulated Gene Networks in a Temporal Lobe Epilepsy Model.
Article in Annals of neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Obesity Aggravates Status Epilepticus Through Lipocalin-2-mediated Inflammation and Necroptosis.Neurochemical research · 2026Article
- STAT3 signaling is associated with neuroimmune dysregulation in a Dravet syndrome model and pediatric drug-resistant epilepsy.Frontiers in neuroscience · 2026Article
- Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026Review
- Beyond mTOR: Unraveling the Complex Pathophysiology and Signaling Pathways in Focal Cortical Dysplasia.Molecular neurobiology · 2025Review
- Chronic 40 Hz light flicker mitigates epileptogenesis through a visual pathway associated with the dorsal lateral geniculate nucleus shell.Nature communications · 2025Article
- Triptolide Inhibits Epileptic Seizures by Rescuing the Neuroinflammation-Related GABAergic Dysfunction in Mice.CNS neuroscience & therapeutics · 2025Article
- Investigating the Potential Therapeutic Targeting of the JAK-STAT Pathway in Cerebrovascular Diseases: Opportunities and Challenges.Molecular neurobiology · 2025Review
- Calpastatin, a calpain specific inhibitor, reduce seizures in a mouse model of temporal lobe epilepsy.Epilepsia open · 2025Article
- Disease modification upon 2 weeks of tofacitinib treatment in a mouse model of chronic epilepsy.Science translational medicine · 2025Article
- Ruxolitinib-dependent reduction of seizure load and duration is accompanied by spatial memory improvement in the rat pilocarpine model of temporal lobe epilepsy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- CPEB3 can regulate seizure susceptibility by inhibiting the transcriptional activity of STAT3 on NMDARs expression.Molecular medicine (Cambridge, Mass.) · 2025Article
- Research progress on the role of inflammatory mediators in the pathogenesis of epilepsy.Ibrain · 2025Review
- Contribution of the Activated mTOR-STAT3 Pathway to the Pathogenesis of Focal Cortical Dysplasia Type IIIa in Pediatric Patients through Astrocyte Proliferation Mediation.Current molecular medicine · 2025Article
- Infantile Spasms in Pediatric Down Syndrome: Potential Mechanisms Driving Therapeutic Considerations.Children (Basel, Switzerland) · 2024Review
- Unraveling the Neural Circuits: Techniques, Opportunities and Challenges in Epilepsy Research.Cellular and molecular neurobiology · 2024Review
- Blocking salt-inducible kinases with YKL-06-061 prevents PTZ-induced seizures in mice.Brain and behavior · 2023Article
- Janus kinase inhibitors are potential therapeutics for amyotrophic lateral sclerosis.Translational neurodegeneration · 2023Review
- miR-98-5p Prevents Hippocampal Neurons from Oxidative Stress and Apoptosis by Targeting STAT3 in Epilepsy in vitro.Neuropsychiatric disease and treatment · 2023Article
- Epileptic Neurons Know JAK/STAT3.Epilepsy currentsArticle
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveTemporal lobe epilepsy (TLE) is a progressive disorder mediated by pathological changes in molecular cascades and hippocampal neural circuit remodeling that results in spontaneous seizures and cognitive dysfunction. Targeting these cascades may provide disease-modifying treatments for TLE patients. Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) inhibitors have emerged as potential disease-modifying therapies; a more detailed understanding of JAK/STAT participation in epileptogenic responses is required, however, to increase the therapeutic efficacy and reduce adverse effects associated with global inhibition.
methodsWe developed a mouse line in which tamoxifen treatment conditionally abolishes STAT3 signaling from forebrain excitatory neurons (nSTAT3KO). Seizure frequency (continuous in vivo electroencephalography) and memory (contextual fear conditioning and motor learning) were analyzed in wild-type and nSTAT3KO mice after intrahippocampal kainate (IHKA) injection as a model of TLE. Hippocampal RNA was obtained 24 h after IHKA and subjected to deep sequencing.
resultsSelective STAT3 knock-out in excitatory neurons reduced seizure progression and hippocampal memory deficits without reducing the extent of cell death or mossy fiber sprouting induced by IHKA injection. Gene expression was rescued in major networks associated with response to brain injury, neuronal plasticity, and learning and memory. We also provide the first evidence that neuronal STAT3 may directly influence brain inflammation.
interpretationInhibiting neuronal STAT3 signaling improved outcomes in an animal model of TLE, prevented progression of seizures and cognitive co-morbidities while rescuing pathogenic changes in gene expression of major networks associated with epileptogenesis. Specifically targeting neuronal STAT3 may be an effective disease-modifying strategy for TLE. ANN NEUROL 2023;94:106-122.
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