ArticleCell death & disease2019
TRAF2 protects against cerebral ischemia-induced brain injury by suppressing necroptosis.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 81 citations in OpenAlex.
- Small-molecule-induced neuron-specific hypoxia: recapitulating developmental angiogenesis for ischemic stroke therapy.Acta pharmacologica Sinica · 2026Article
- Shh-S100A10 axis curbs neuronal PANoptosis after ischemic stroke.Neural regeneration research · 2026Article
- Research Prospects for Necroptosis in Inflammatory Diseases: A Bibliometric Analysis.Current medicinal chemistry · 2026Review
- HAT1 Protects Against Cerebral Ischemia Injury by Inhibiting TFRC-Mediated Ferroptosis.Neurochemical research · 2025Article
- Myocardial mitochondrial antiviral signaling protein promotes heart Ischemia-reperfusion injury via RIG-I signaling in mice.Nature communications · 2025Article
- Identification of NETs-related genes as diagnostic biomarkers in ischemic stroke using RNA sequencing and single-cell analysis.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- LncRNA MEG3 promotes pyroptosis via miR-145-5p/TLR4/NLRP3 axis and aggravates cerebral ischemia-reperfusion injury.Metabolic brain disease · 2025Article
- VX-765 alleviates motor and cognitive impairments via inhibiting PANoptosis activation in the neonatal rats after hypoxic-ischemic brain damage.Pediatric discovery · 2025Article
- Noncanonical feedback loop between "RIP3-MLKL" and "4EBP1-eIF4E" promotes neuronal necroptosis.MedComm · 2025Article
- Article
- Hypoxia-mediated SUMOylation of FADD exacerbates endothelial cell injury via the RIPK1-RIPK3-MLKL signaling axis.Cell death & disease · 2025Article
- Progress in Research on Regulated Cell Death in Cerebral Ischaemic Injury After Cardiac Arrest.Journal of cellular and molecular medicine · 2025Review
- Constructing methylation-driven ceRNA networks unveil tumor heterogeneity and predict patient prognosis.Human molecular genetics · 2025Article
- TRAF2 and RIPK1 redundantly mediate classical NFκB signaling by TNFR1 and CD95-type death receptors.Cell death & disease · 2025Article
- Cerebral ischemia-reperfusion injury: mechanisms and promising therapies.Frontiers in pharmacology · 2025Review
- Ripks and Neuroinflammation.Molecular neurobiology · 2024Review
- The Role of Necroptosis in Cerebral Ischemic Stroke.Molecular neurobiology · 2024Review
- Regulated cell death in hypoxic-ischaemic encephalopathy: recent development and mechanistic overview.Cell death discovery · 2024Review
- Ubiquitous regulation of cerebrovascular diseases by ubiquitin-modifying enzymes.Clinical and translational medicine · 2024Review
- Intranasal Delivery of Anti-Apoptotic siRNA Complexed with Fas-Signaling Blocking Peptides Attenuates Cellular Apoptosis in Brain Ischemia.Pharmaceutics · 2024Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis contributes to ischemia-induced brain injury. Tumor necrosis factor (TNF) receptor associated factor 2 (TRAF2) has been reported to suppress necroptotic cell death under several pathological conditions. In this study, we investigated the role of TRAF2 in experimental stroke using a mouse middle cerebral artery occlusion (MCAO) model and in vitro cellular models. TRAF2 expression in the ischemic brain was assessed with western blot and real-time RT-PCR. Gene knockdown of TRAF2 by lentivirus was utilized to investigate the role of TRAF2 in stroke outcomes. The expression of TRAF2 was significantly induced in the ischemic brain at 24 h after reperfusion, and neurons and microglia were two of the cellular sources of TRAF2 induction. Striatal knockdown of TRAF2 increased infarction size, cell death, microglial activation and the expression of pro-inflammatory markers at 24 h after reperfusion. TRAF2 expression and necroptosis were induced in mouse primary microglia treated with conditioned medium collected from neurons subject to oxygen and glucose deprivation (OGD) and in TNFα-treated mouse hippocampal neuronal HT-22 cells in the presence of the pan-caspase inhibitor Z-VAD. In addition, TRAF2 knockdown exacerbated microglial cell death and neuronal cell death under these conditions. Moreover, pre-treatment with a specific necroptosis inhibitor necrostatin-1 (nec-1) suppressed the cell death exacerbated by TRAF2 knockdown in the brain following MCAO, indicating that TRAF2 impacted ischemic brain damage through necroptosis mechanism. Taken together, our results demonstrate that TRAF2 is a novel regulator of cerebral ischemic injury.
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