ArticleJournal of neuroinflammation2023
GSDMD knockdown attenuates phagocytic activity of microglia and exacerbates seizure susceptibility in TLE mice.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 21 citations in OpenAlex.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- 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
- Gasdermin D in Neurodegenerative Diseases: Pathogenic Roles and Therapeutic Perspectives.Molecular neurobiology · 2026Review
- Neuroinflammation promotes the development of pharmacoresistant epilepsy by triggering the MSK1/CREB signaling pathway.Scientific reports · 2026Article
- GASDERMIN D-mediated pyroptosis as a therapeutic target in TAU-dependent frontotemporal dementia mouse model.Journal of biomedical science · 2026Article
- Pyroptosis in epilepsy: from pathophysiological mechanisms to therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- A vicious cycle of microglial dysfunction: bridging synaptic pruning and neuroinflammation across the neurodevelopmental continuum.Frontiers in immunology · 2026Review
- The Evolving Role of Mesenchymal Stem Cells and Their Exosomes in Epilepsy Management: From Bench to Bedside.Stem cells international · 2026Review
- Anti-epileptic effect of saikosaponin a by inhibiting ferroptosis via the IL-17/Akt/ERK signaling pathway in the temporal lobe epilepsy model.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The interplay between metabolism and neuroinflammation in epilepsy: mechanisms and therapeutic perspectives.Journal of neuroinflammation · 2025Review
- Neuronal regulated cell death in aging-related neurodegenerative diseases: key pathways and therapeutic potentials.Neural regeneration research · 2025Article
- Effects of ATF2/TSC1 on epilepsy by modulating the microphages polarization of microglia.Scientific reports · 2025Article
- Article
- LncRNA-GPHN Regulates Epilepsy by Inhibiting Apoptosis via the miR-320/YWHAH Axis in an Immature Rat Model of Status Epilepticus.Journal of cellular and molecular medicine · 2025Article
- Microglia efferocytosis: an emerging mechanism for the resolution of neuroinflammation in Alzheimer's disease.Journal of neuroinflammation · 2025Review
- Exploratory analysis of a Novel RACK1 mutation and its potential role in epileptic seizures via Microglia activation.Journal of neuroinflammation · 2025Article
- Role of inflammasomes and neuroinflammation in epilepsy.Immunological reviews · 2025Review
- Levetiracetam Prevents Neurophysiological Changes and Preserves Cognitive Function in the Human Immunodeficiency Virus (HIV)-1 Transactivator of Transcription Transgenic Mouse Model of HIV-Associated Neurocognitive Disorder.The Journal of pharmacology and experimental therapeutics · 2024Article
- Mitochondrial ferritin alleviates ferroptosis in a kainic acid-induced mouse epilepsy model by regulating iron homeostasis: Involvement of nuclear factor erythroid 2-related factor 2.CNS neuroscience & therapeutics · 2024Article
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundTemporal lobe epilepsy (TLE) is often characterized pathologically by severe neuronal loss in the hippocampus. Phagocytic activity of microglia is essential for clearing apoptotic neuronal debris, allowing for repair and regeneration. Our previous research has shown that gasdermin D (GSDMD)-mediated pyroptosis is involved in the pathogenesis of TLE. However, whether GSDMD-mediated pyroptosis influences the accumulation of apoptotic neurons remains unclear. Therefore, the present study was designed to investigate whether phagocytic activity of microglia is involved in GSDMD-mediated pyroptosis and the pathogenesis of TLE.
methodsTo establish a TLE model, an intra-amygdala injection of kainic acid (KA) was performed. The Racine score and local field potential (LFP) recordings were used to assess seizure severity. Neuronal death in the bilateral hippocampus was assessed by Nissl staining and TUNEL staining. Microglial morphology and phagocytic activity were detected by immunofluorescence and verified by lipopolysaccharide (LPS) and the P2Y
resultsGSDMD knockdown augmented the accumulation of apoptotic neurons and seizure susceptibility in TLE mice. Microglia activated and transition to the M1 type with increased pro-inflammatory cytokines. Furthermore, GSDMD knockdown attenuated the migration and phagocytic activity of microglia. Of note, LPS-activated microglia attenuated seizure susceptibility and the accumulation of apoptotic neurons in TLE after GSDMD knockdown. A P2Y
conclusionsOur results demonstrate that GSDMD knockdown exacerbates seizure susceptibility and the accumulation of apoptotic neurons by attenuating phagocytic activity of microglia. These findings suggest that GSDMD plays a protective role against KA-induced seizure susceptibility.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.