ArticleExperimental & molecular medicine2022
TRIM45 causes neuronal damage by aggravating microglia-mediated neuroinflammation upon cerebral ischemia and reperfusion injury.
Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 123 citations in OpenAlex.
- TAB2 Causes Neuronal Damage by Aggravating Microglia-Mediated Neuroinflammation in Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Dysfunction of hippocampal cells and its role in cognitive impairment.Neural regeneration research · 2026Article
- MST1/Drp1 axis mediates microglia pro-inflammatory activation following cerebral ischemia-reperfusion injury.Scientific reports · 2026Article
- NFAT1Cellular & molecular biology letters · 2026Article
- Neural stem cell-derived exosomal PA2G4 induces ANXA2 degradation to promote mitophagy and alleviate neuronal oxidative stress in cerebral ischemia/reperfusion.Apoptosis : an international journal on programmed cell death · 2026Article
- IGF2BP1 Aggravates NLRP3 Inflammasome Activation and Pro-Inflammatory Phenotype in Microglia-like Cells by Promoting TRIM45 Expression.Neurotoxicity research · 2026Article
- Roles and Mechanisms of TRIM Family Proteins in Inflammation in the Brain and Beyond.International journal of molecular sciences · 2026Review
- TRIM21 Exacerbates Ischemic Brain Injury by Promoting Astrocyte-Mediated Neuroinflammation via K63-Linked Ubiquitination of MDA5.Research (Washington, D.C.) · 2026Article
- Dual regulation of Atf3 and Lonp1 as therapeutic targets in cerebral ischaemia-reperfusion injury.Stroke and vascular neurology · 2025Article
- Comprehensive analysis of immune escape-related prognostic signature in high-grade glioma.Discover oncology · 2025Article
- USP43 promotes cerebral ischemia-reperfusion injury via activation of TAK1.Cell & bioscience · 2025Article
- A study on the mechanism of Bushen Kaiqiao Formula in modulating microglial activation to alleviate neuroinflammation in ADHD.Biochemistry and biophysics reports · 2025Article
- TargetingJournal of pharmaceutical analysis · 2025Article
- Immunological Mechanisms and Therapeutic Strategies in Cerebral Ischemia-Reperfusion Injury: From Inflammatory Response to Neurorepair.International journal of molecular sciences · 2025Review
- Oseltamivir Phosphate Modulates CD24-Siglec-G/10 Interaction to Suppress Microglial-Driven Neuroinflammation After Cardiac Arrest.CNS neuroscience & therapeutics · 2025Article
- The Roles of E3 Ubiquitin Ligases in Cerebral Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
- BMSCs-derived exosomal Egr2 inhibited OGD/R-induced neuronal cell injury through the RNF8/DAPK1 axis in ischemic stroke.Experimental brain research · 2025Article
- The autocrine motility factor receptor delays the pathological progression of Alzheimer's disease via regulating the ubiquitination-mediated degradation of APP.Alzheimer's research & therapy · 2025Article
- Deubiquitination of RIPK3 by OTUB2 potentiates neuronal necroptosis after ischemic stroke.EMBO molecular medicine · 2025Article
- E2F1/CDK5/DRP1 axis mediates microglial mitochondrial division and autophagy in the pathogenesis of cerebral ischemia-reperfusion injury.Clinical and translational medicine · 2025Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Excessive and unresolved neuroinflammation is a key component of the pathological cascade in brain injuries such as ischemic stroke. Tripartite motif-containing 45 (TRIM45) is a ubiquitin E3 ligase involved in various critical biological processes. However, the role of TRIM45 in cerebral ischemia remains unknown. Here, we found that the TRIM45 protein was highly expressed in the peri-infarct areas of mice subjected to cerebral ischemia and reperfusion injury induced by middle cerebral artery occlusion. This study systemically evaluated the putative role of TRIM45 in the regulation of neuroinflammation during ischemic injury and the potential underlying mechanisms. We found that TRIM45 knockdown significantly decreased proinflammatory cytokine and chemokine production in primary cultured microglia challenged with oxygen-glucose deprivation and reoxygenation (OGD/R) treatment. Mechanistically, we demonstrated that TRIM45 constitutively interacted with TAB2 and consequently facilitated the Lys-63-linked polyubiquitination of TAB2, leading to the formation of the TAB1-TAK1-TAB2 complex and activation of TAK1, which was ultimately followed by activation of the nuclear factor-kappa B (NF-κB) signaling pathway. In an in vitro coculture Transwell system, downregulation of TRIM45 expression also inhibited the OGD/R-induced activation of microglia and alleviated neuronal apoptosis. More importantly, microglia-specific knockdown of TRIM45 in mice significantly reduced the infarct size, mitigated neurological deficit scores, and improved cognitive function after ischemic stroke. Taken together, our study reveals that the TRIM45-TAB2 axis is a crucial checkpoint that controls NF-κB signaling in microglia during cerebral ischemia and reperfusion injury. Therefore, targeting TRIM45 may be an attractive therapeutic strategy.
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