ArticleBrain and behavior2024
LncRNA ILF3-AS1 mediates oxidative stress and inflammation through miR-504-3p/HMGB1 axis in a cellular model of temporal lobe epilepsy.
Article in Brain and behavior, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Carvedilol attenuates PTZ-induced epileptogenesis: associations with hippocampal neuroinflammation and PI3K/AKT/mTOR-related alterations.Scientific reports · 2026Article
- β-hydroxybutyrate regulates microglia M1/M2 polarization and phagocytosis through the JAK1/STAT1 pathway to reduce neuroinflammation and exert anti-epileptic effects.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Improving epilepsy management by targeting P2 × 7 receptor with ROS/electric responsive nanomicelles.Journal of nanobiotechnology · 2025Article
- Altered Neuroplasticity in Epilepsy is Associated with Neuroinflammation and Oxidative Stress: In vivo Evidence of Brain-Derived Extracellular Vesicles.International journal of nanomedicine · 2025Article
- Silencing epileptic storms: targeting miRNA-lncRNA crosstalk in astrocytes and microglia to disarm neuroinflammatory triggers.Frontiers in molecular neuroscience · 2025Review
- LncRNA ILF3-AS1 mediates oxidative stress and inflammation through miR-504-3p/HMGB1 axis in a cellular model of temporal lobe epilepsy.Brain and behavior · 2024Article
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Authors and funding
3 authors.
Funding
Abstract
backgroundTemporal lobe epilepsy (TLE), a prevalent neurological disorder, is associated with hippocampal oxidative stress and inflammation. A recent study reveals that the long noncoding RNA ILF3 divergent transcript (ILF3-AS1) level is elevated in the hippocampus of TLE patients; however, the functional roles of ILF3-AS1 in TLE and underlying mechanisms deserve further investigation. Hence, this study aimed to elucidate whether ILF3-AS1 is involved in the pathogenesis of TLE by regulating oxidative stress and inflammation and to explore its underlying mechanism in vitro.
methodsHuman hippocampal neurons were subjected to a magnesium-free (Mg
resultsIn Mg
conclusionOur findings indicate that ILF3-AS1 contributes to Mg
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Registered trials
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