<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>37(10)</volume><submitter>Jiang GT</submitter><pubmed_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 exace</pubmed_abstract><journal>Neuroscience bulletin</journal><pagination>1427-1440</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8490607</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Complement C3 Aggravates Post-epileptic Neuronal Injury Via Activation of TRPV1.</pubmed_title><pmcid>PMC8490607</pmcid><pubmed_authors>Shao L</pubmed_authors><pubmed_authors>Cheng JJ</pubmed_authors><pubmed_authors>Han S</pubmed_authors><pubmed_authors>Chen TX</pubmed_authors><pubmed_authors>Peng BW</pubmed_authors><pubmed_authors>Gongga L</pubmed_authors><pubmed_authors>Liu YM</pubmed_authors><pubmed_authors>Liu WH</pubmed_authors><pubmed_authors>He XH</pubmed_authors><pubmed_authors>Jiang GT</pubmed_authors><pubmed_authors>Kong S</pubmed_authors><pubmed_authors>Zeng ML</pubmed_authors><pubmed_authors>Yin J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Complement C3 Aggravates Post-epileptic Neuronal Injury Via Activation of TRPV1.</name><description>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 exace</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Oct</publication><modification>2026-06-01T02:23:47.228Z</modification><creation>2025-04-05T20:44:18.629Z</creation></dates><accession>S-EPMC8490607</accession><cross_references><pubmed>34309810</pubmed><doi>10.1007/s12264-021-00750-4</doi></cross_references></HashMap>