ArticleCNS neuroscience & therapeutics2024
GLS2 reduces the occurrence of epilepsy by affecting mitophagy function in mouse hippocampal neurons.
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 8 papers.
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8 citing papers in PubMed.
- Mitochondria transfer in neurological disorders: the key role of neuroglia.Molecular neurodegeneration · 2026Review
- NR4A3 alleviates diabetic neuropathy via GLS2-mediated mitochondrial repair and Schwann cell differentiation.iScience · 2026Article
- ANXA2 promotes NLRP3 inflammasome activation and neuronal pyroptosis after intracerebral hemorrhage.Frontiers in immunology · 2026Article
- The Role of GABA Pathway Components in Pathogenesis of Neurodevelopmental Disorders.International journal of molecular sciences · 2025Review
- JC124 confers multimodal neuroprotection in epilepsy by suppressing NLRP3 inflammasome activation: evidence from animal and human neuronal models.Cell communication and signaling : CCS · 2025Article
- Neurotransmission Sex Dichotomy in the Rat Hypothalamic Paraventricular Nucleus in Healthy and Infantile Spasm Model.Current issues in molecular biology · 2025Article
- NLRP3 inflammasome inhibits mitophagy during the progression of temporal lobe epilepsy.Scientific reports · 2025Article
- GLS2 reduces the occurrence of epilepsy by affecting mitophagy function in mouse hippocampal neurons.CNS neuroscience & therapeutics · 2024Article
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13 authors.
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Abstract
backgroundAltered mitophagy has been observed in various neurological disorders, such as epilepsy. The role of mitophagy in causing neuronal damage during epileptic episodes is significant, and recent research has indicated that GLS2 plays a crucial role in regulating autophagy. However, exactly how GLS2 affects epilepsy is still unclear.
aimsTo investigate the expression and distribution characteristics of GLS2 in epilepsy, and then observed the changes in behavior and electrophysiology caused by overexpression of GLS2 in epileptic mice, and determined whether GLS2 regulated seizure-like changes in the mouse model through the protective mechanism of mitophagy.
resultsThe expression of GLS2 in a kainic acid (KA)-induced epileptic mouse model and aglutamate-inducedneuronal excitatory damage in HT22 cells model was downregulation. In brief, overexpression of GLS2 can alleviate epileptic activity. Subsequently, we demonstrated that GLS2 interacts with mitophagy-related proteins in a KA-induced epilepsy mouse model. Mechanistically, overexpression of GLS2 inhibited mitophagy in epileptic mice, downregulating the expression of LC3 and reducing ROS production.
conclusionsThis study proves the GLS2 expression pattern is abnormal in epileptic mice. The function of mitophagy in hippocampal neurons is affected by GLS2, and overexpression of GLS2 can reduce the occurrence of seizure-like events (SLEs) by altering mitophagy function. Thus, GLS2 might control seizures, and our findings provide a fresh avenue for antiepileptic treatment and offer novel insights into treating and preventing epilepsy.
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