ArticleBrain circulation
Glycogen synthase kinase-3β mediates toll-like receptors 4/nuclear factor kappa-B-activated cerebral ischemia-reperfusion injury through regulation of fat mass and obesity-associated protein.
Article in Brain circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Function of the large intestine and its interaction with the brain after ischemic stroke: a comprehensive literature review.Frontiers in cellular neuroscience · 2026Review
- Pre-thrombectomy cerebral edema affects outcomes in acute stroke patients treated with thrombectomy.International journal of medical sciences · 2025Article
- Steroids' Neuroprotective Potential in Severe Cerebral Venous Thrombosis: Experimental and Clinical Exploration of NLRP3 Inflammasome Inhibition.CNS neuroscience & therapeutics · 2024Article
- Multi-Target and Multi-Phase Adjunctive Cerebral Protection for Acute Ischemic Stroke in the Reperfusion Era.Biomolecules · 2024Review
- Prospective randomized controlled trial on the safety and neuroprotective efficacy of remote administration of hypothermia over spleen during acute ischemic stroke with mechanical thrombectomy: rationale, design, and protocol.Frontiers in neurology · 2024Article
- The impact of high-altitude and cold environment on brain and heart damage in rats with hemorrhagic shock.Brain circulationArticle
- A novel mucosa-associated lymphoid tissue translocation gene 1-related immune prognostic signature and targeted drug screening for glioblastoma.Brain circulationArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlycogen synthase kinase-3β (GSK3β), fat mass and obesity-associated protein (FTO), and toll-like receptors 4 (TLR4) take on critical significance in different biological processes, whereas their interactions remain unclear. The objective was the investigation of the interaction effect in cerebral ischemia-reperfusion (I/R) injury.
methodsThe function of the cerebral cortex in the mouse middle cerebral artery occlusion (MCAO) model (each group
resultsAfter GSK3β knockdown in the OGD/R model of PC12 cells, the levels of TLR4 and p-p65 were lower than in the control, and the level of FTO was higher than in the control. Knockdown GSK3β reversed the OGD/R-induced nuclear factor kappa-B transfer to the intranuclear nuclei. As indicated by the result, TLR4 expression was down-regulated by overexpressed FTO, and TLR4 expression was up-regulated notably after inhibition of FTO with the use of R-2HG. After the inhibition of the activity of GSK3β
conclusionsOur research shows that GSK3β/FTO/TLR4 pathway contributes to cerebral I/R injury.
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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.