ArticleFrontiers in molecular neuroscience2011
Regulation by glycogen synthase kinase-3 of inflammation and T cells in CNS diseases.
Article in Frontiers in molecular neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 82 citations in OpenAlex.
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- Role of GSK-3β Inhibitors: New Promises and Opportunities for Alzheimer's Disease.Advanced pharmaceutical bulletin · 2023Review
- The role of glycogen synthase kinase 3 beta in neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
- Sepsis-associated brain injury: underlying mechanisms and potential therapeutic strategies for acute and long-term cognitive impairments.Journal of neuroinflammation · 2022Review
- Electroacupuncture improves TBI dysfunction by targeting HDAC overexpression and BDNF-associated Akt/GSK-3β signaling.Frontiers in cellular neuroscience · 2022Article
- Immune Signaling Kinases in Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD).International journal of molecular sciences · 2021Review
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- IGF-1 Alleviates Mitochondrial Apoptosis through the GSK3β/NF-κB/NLRP3 Signaling Pathway in LPS-Treated PC-12 Cells.Journal of molecular neuroscience : MN · 2021Article
- Extracellular Vesicle Proteins and MicroRNAs Are Linked to Chronic Post-Traumatic Stress Disorder Symptoms in Service Members and Veterans With Mild Traumatic Brain Injury.Frontiers in pharmacology · 2021Article
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- Insight into glycogen synthase kinase-3β inhibitory activity of phyto-constituents fromIn silico pharmacology · 2020Article
- GSK-3β Contributes to Parkinsonian Dopaminergic Neuron Death: Evidence From Conditional Knockout Mice and Tideglusib.Frontiers in molecular neuroscience · 2020Article
- miR-1185-1 and miR-548q Are Biomarkers of Response to Weight Loss and Regulate the Expression ofCells · 2019Article
- Glycogen synthase kinase-3β inhibition enhances myelination in preterm newborns with intraventricular hemorrhage, but not recombinant Wnt3A.Neurobiology of disease · 2018Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Elevated markers of neuroinflammation have been found to be associated with many psychiatric and neurodegenerative diseases, such as mood disorders, Alzheimer's disease, and multiple sclerosis (MS). Since neuroinflammation is thought to contribute to the pathophysiology of these diseases and to impair responses to therapeutic interventions and recovery, it is important to identify mechanisms that regulate neuroinflammation and potential targets for controlling neuroinflammation. Recent findings have demonstrated that glycogen synthase kinase-3 (GSK3) is an important regulator of both the innate and adaptive immune systems' contributions to inflammation. Studies of the innate immune system have shown that inhibitors of GSK3 profoundly alter the repertoire of cytokines that are produced both by peripheral and central cells, reducing pro-inflammatory cytokines, and increasing anti-inflammatory cytokines. Furthermore, inhibitors of GSK3 promote tolerance to inflammatory stimuli, reducing inflammatory cytokine production upon repeated exposure. Studies of the adaptive immune system have shown that GSK3 regulates the production of cytokines by T cells and the differentiation of T cells to subtypes, particularly Th17 cells. Regulation of transcription factors by GSK3 appears to play a prominent role in its regulation of immune responses, including of NF-κB, cyclic AMP response element binding protein, and signal transducer and activator of transcription-3. Invivo studies have shown that GSK3 inhibitors ameliorate clinical symptoms of both peripheral and central inflammatory diseases, particularly experimental autoimmune encephalomyelitis, the animal model of MS. Therefore, the development and application of GSK3 inhibitors may provide a new therapeutic strategy to reduce neuroinflammation associated with many central nervous system diseases.
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