ReviewFrontiers in molecular neuroscience2022
Inhibition of glycogen synthase kinase 3 by lithium, a mechanism in search of specificity.
Review in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 47 citations in OpenAlex.
- Fgk3 interacts with FgMetR to regulate mycelial growth, conidia development, DON production, and pathogenicity in Fusarium graminearum.Stress biology · 2026Article
- LiCl induces GSK-3β mediated autophagy, DNA damage, and cell cycle arrest in HPV driven cervical cancer cells.Cancer chemotherapy and pharmacology · 2026Article
- Lithium as a Potential Senostatic Agent in Central Nervous System Aging and Bipolar Disorder.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Clinical Significance and Changes in Levels of Serum BDNF, mBDNF, AQP4, proBDNF, and GSK3β in Individuals Diagnosed With Bipolar Disorder: A Cross-Sectional Study.Health science reports · 2026Article
- Extracellular stressors change BBSome expression of benign mesothelial and primary pleural mesothelioma cells and affect cell adhesion and migration.Physiological reports · 2026Article
- Targeting the GSK-3β/mTOR axis: a novel pharmacological strategy for preeclampsia prevention and treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Glycogen Synthase Kinase-3β Mediates Suppression of Neurite Outgrowth Through Sonic Hedgehog Signalling in Palmitic Acid-Exposed Neuro2A Cells.Molecular neurobiology · 2026Article
- Baseline NMR lipoprotein profiles in lithium-naïve bipolar disorder patients who later showed weight gain during lithium therapy: a pilot study.International journal of bipolar disorders · 2026Article
- Genetic Polymorphisms Associated with Lithium Response in Bipolar Disorder: An Integrative Review and In Silico Protein-Protein Interaction Analysis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- No evidence lithium supplementation extends lifespan in male Drosophila melanogaster.Biogerontology · 2026Article
- Lithium Therapeutic Functions: An Update on Pharmacokinetics, Pathophysiological Mechanisms of Action, Toxicity, and Side Effects.Molecular neurobiology · 2026Review
- Assessment of the biological efficacy of gold Nannochloropsis oculata nano-extract against lithium-induced toxicity in rats.Scientific reports · 2026Article
- Molecular interplay between glycogen synthase kinase 3 beta and A-kinase anchoring protein 11 in bipolar disorder: a narrative review.Frontiers in molecular neuroscience · 2026Review
- Engram cell vulnerability in neurodegeneration: from mechanistic insights to therapeutic horizons.Frontiers in aging neuroscience · 2026Review
- Article
- Glycogen synthase kinase-3: the master switch driving neurodegeneration in Alzheimer's disease and Parkinson's disease.Archives of toxicology · 2025Review
- Computational Modeling of PI3K/AKT Pathway in Bipolar Disorder and Type 2 Diabetes: Implications for Lithium Treatment and Curcumin as a Potential Alternative.International journal of molecular sciences · 2025Article
- Lithium Augmentation in Treatment-Resistant Depression: A Qualitative Review of the Literature.Pharmacotherapy · 2025Review
- The crosstalk between CREB and PER2 mediates the transition between mania- and depression-like behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Acute and reversible dyskinesias secondary to lithium toxicity: case report and literature review.BMC neurology · 2025Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibition of Glycogen synthase kinase 3 (GSK3) is a popular explanation for the effects of lithium ions on mood regulation in bipolar disorder and other mental illnesses, including major depression, cyclothymia, and schizophrenia. Contribution of GSK3 is supported by evidence obtained from animal and patient derived model systems. However, the two GSK3 enzymes, GSK3α and GSK3β, have more than 100 validated substrates. They are thus central hubs for major biological functions, such as dopamine-glutamate neurotransmission, synaptic plasticity (Hebbian and homeostatic), inflammation, circadian regulation, protein synthesis, metabolism, inflammation, and mitochondrial functions. The intricate contributions of GSK3 to several biological processes make it difficult to identify specific mechanisms of mood stabilization for therapeutic development. Identification of GSK3 substrates involved in lithium therapeutic action is thus critical. We provide an overview of GSK3 biological functions and substrates for which there is evidence for a contribution to lithium effects. A particular focus is given to four of these: the transcription factor cAMP response element-binding protein (CREB), the RNA-binding protein FXR1, kinesin subunits, and the cytoskeletal regulator CRMP2. An overview of how co-regulation of these substrates may result in shared outcomes is also presented. Better understanding of how inhibition of GSK3 contributes to the therapeutic effects of lithium should allow for identification of more specific targets for future drug development. It may also provide a framework for the understanding of how lithium effects overlap with those of other drugs such as ketamine and antipsychotics, which also inhibit brain GSK3.
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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.