ArticleRedox biology2024
Glucose-6-phosphate dehydrogenase alleviates epileptic seizures by repressing reactive oxygen species production to promote signal transducer and activator of transcription 1-mediated N-methyl-d-aspartic acid receptors inhibition.
Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Enhanced Glycolysis-Driven Histone H3K18 Lactylation Regulates Epileptogenesis by Modulating the E3 Ubiquitin Ligase COP1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Decorin Attenuates Epileptogenesis and Modulates Hippocampal Synaptic Plasticity via the mTOR Signalling Pathway.Neurochemical research · 2026Article
- Abnormal glycosylation changes in brain tissue of kainic acid-induced epileptic rats.Scientific reports · 2025Article
- Permethrin induces epileptic susceptibility via activation of NaCommunications biology · 2025Article
- Correlation between metabolism and neuroinflammation of astrocytes in drug-resistant epilepsy.Journal of neurology · 2025Review
- Review
- Clinical updates of JAK inhibitors in cutaneous granulomatous diseases.Frontiers in immunology · 2025Review
- Evaluating seizures associated with novel antineoplastic agents during breast cancer treatment using the Food and Drug Administration Adverse Event Reporting System and Canada Vigilance Adverse Reaction Online Database.Therapeutic advances in drug safety · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of epilepsy remains unclear; however, a prevailing hypothesis suggests that the primary underlying cause is an imbalance between neuronal excitability and inhibition. Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme in the pentose phosphate pathway, which is primarily involved in deoxynucleic acid synthesis and antioxidant defense mechanisms and exhibits increased expression during the chronic phase of epilepsy, predominantly colocalizing with neurons. G6PD overexpression significantly reduces the frequency and duration of spontaneous recurrent seizures. Furthermore, G6PD overexpression enhances signal transducer and activator of transcription 1 (STAT1) expression, thus influencing N-methyl-d-aspartic acid receptors expression, and subsequently affecting seizure activity. Importantly, the regulation of STAT1 by G6PD appears to be mediated primarily through reactive oxygen species signaling pathways. Collectively, our findings highlight the pivotal role of G6PD in modulating epileptogenesis, and suggest its potential as a therapeutic target for epilepsy.
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