ArticleNeuroscience bulletin2021
Complement C3 Aggravates Post-epileptic Neuronal Injury Via Activation of TRPV1.
Article in Neuroscience bulletin, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Immune-mediated excitotoxicity in brain disorders.Nature reviews. Immunology · 2026Review
- Prednisone Exposure During Pregnancy Increases Susceptibility to Epilepsy in Adult Offspring Mice.Neurochemical research · 2026Article
- Astrocytes in Genetic Epilepsies: Supporting Actor or Key Player?Journal of neuroscience research · 2026Review
- A biomimetic cryoprotectant preserves extracellular vesicles bioactivity for intravenous administration and potentiates wound healing.Journal of nanobiotechnology · 2026Article
- The complement C3-microglial axis in depression of Parkinson's disease: from mechanism to therapeutic intervention.EBioMedicine · 2026Article
- NGF-Hydrogel Ameliorates Aberrant Adult Hippocampal Neurogenesis and Improves Hippocampal Remodeling After Epilepsy.Current issues in molecular biology · 2026Article
- TPPU protects against seizures and seizure-associated comorbidities by inhibiting the Akt/mTOR signaling pathway in KA-induced convulsant mice.Frontiers in immunology · 2026Article
- Pathophysiology of Status Epilepticus Revisited.International journal of molecular sciences · 2025Review
- Dynamic astrocytic complement C3 activation in the epileptic hippocampus.Frontiers in neurology · 2025Article
- Treadmill Exercise Reshapes Cortical Astrocytic and Neuronal Activity to Improve Motor Learning Deficits Under Chronic Alcohol Exposure.Neuroscience bulletin · 2024Article
- Blockade of mesenteric and omental adipose tissue sensory neurons improves cardiac remodeling through sympathetic pathway.iScience · 2024Article
- Interleukins in Epilepsy: Friend or Foe.Neuroscience bulletin · 2024Review
- Treadmill exercise improves hippocampal neural plasticity and relieves cognitive deficits in a mouse model of epilepsy.Neural regeneration research · 2024Article
- Changes in the Dentate Gyrus Gene Expression Profile Induced by Levetiracetam Treatment in Rats with Mesial Temporal Lobe Epilepsy.International journal of molecular sciences · 2024Article
- Stiff-person syndrome in association with Hashimoto's thyroiditis: a case report.Frontiers in neurology · 2024Article
- Neural Mechanisms Underlying the Coughing Reflex.Neuroscience bulletin · 2023Review
- RGS5 augments astrocyte activation and facilitates neuroinflammation via TNF signaling.Journal of neuroinflammation · 2023Article
- Astrocyte-derived complement C3 is activated in patients with tuberous sclerosis complex and mediates immune injury: an integrated bioinformatics analysis.Translational pediatrics · 2023Article
- Complement C4-deficient mice have a high mortality rate during PTZ-induced epileptic seizures, which correlates with cognitive problems and the deficiency in the expression of Egr1 and other immediate early genes.Frontiers in cellular neuroscience · 2023Article
- TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications.Biomedicines · 2022Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epilepsy is a brain condition characterized by the recurrence of unprovoked seizures. Recent studies have shown that complement component 3 (C3) aggravate the neuronal injury in epilepsy. And our previous studies revealed that TRPV1 (transient receptor potential vanilloid type 1) is involved in epilepsy. Whether complement C3 regulation of neuronal injury is related to the activation of TRPV1 during epilepsy is not fully understood. We found that in a mouse model of status epilepticus (SE), complement C3 derived from astrocytes was increased and aggravated neuronal injury, and that TRPV1-knockout rescued neurons from the injury induced by complement C3. Circular RNAs are abundant in the brain, and the reduction of circRad52 caused by complement C3 promoted the expression of TRPV1 and exacerbated neuronal injury. Mechanistically, disorders of neuron-glia interaction mediated by the C3-TRPV1 signaling pathway may be important for the induction of neuronal injury. This study provides support for the hypothesis that the C3-TRPV1 pathway is involved in the prevention and treatment of neuronal injury and cognitive disorders.
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Registered trials
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