ArticleThe Journal of pathology2016
The β isoform of GSK3 mediates podocyte autonomous injury in proteinuric glomerulopathy.
Article in The Journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 50 citations in OpenAlex.
- Ligustroflavone alleviates chronic kidney disease by inhibiting ferroptosis through the GSK3β/NRF2 signaling pathway.Redox report : communications in free radical research · 2026Article
- Renal glycogen handling in diabetes: A narrative review of diabetic kidney disease pathogenesis.Journal of diabetes investigation · 2026Review
- From a Shared Stress to Cell-Type-Specific Responses: The Heterogeneous Mechanisms of High Glucose-Induced Cellular Senescence in Diabetic Kidney Disease.Journal of diabetes research · 2026Review
- The role of PANoptosis in diabetes and its complications: mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
- Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease.Clinical science (London, England : 1979) · 2025Review
- Elevation of p53 sensitizes obese kidney to adriamycin-induced aberrant lipid homeostasis via repressing HNF4α-mediated FGF21 sensitivity.Journal of advanced research · 2025Article
- GSK3-Driven Modulation of Inflammation and Tissue Integrity in the Animal Model.International journal of molecular sciences · 2024Review
- THSD7A-associated membranous nephropathy involves both complement-mediated and autonomous podocyte injury.Frontiers in pharmacology · 2024Article
- Article
- KIBRA upregulation increases susceptibility to podocyte injury and glomerular disease progression.JCI insight · 2023Article
- Propofol suppresses adipose-derived stem cell progression via PI3K/AKT-Wnt signaling pathway.BMC anesthesiology · 2022Article
- Age-related GSK3β overexpression drives podocyte senescence and glomerular aging.The Journal of clinical investigation · 2022Article
- Pharmacological Melanocortin 5 Receptor Activation Attenuates Glomerular Injury and Proteinuria in Rats With Puromycin Aminonucleoside Nephrosis.Frontiers in physiology · 2022Article
- Permissive effect of GSK3β on profibrogenic plasticity of renal tubular cells in progressive chronic kidney disease.Cell death & disease · 2021Article
- Upregulated LRRC55 promotes BK channel activation and aggravates cell injury in podocytes.The Journal of experimental medicine · 2021Article
- Serum and Glucocorticoid-Inducible Kinase 3/Nedd4-2 Signaling Pathway Participates in Podocyte Injury by Regulating the Stability of Nephrin.Frontiers in physiology · 2021Article
- Proteome and Phosphoproteome Analyses Reveal the Kinase Regulatory Network Involved in Glycogen Synthesis Kinase 3β.Frontiers in genetics · 2021Article
- Molecular Mechanisms of Metal Toxicity in the Pathogenesis of Alzheimer's Disease.Molecular neurobiology · 2021Review
- The complicated role of mitochondria in the podocyte.American journal of physiology. Renal physiology · 2020Article
- GSK3 modulation in acute lung injury, myocarditis and polycystic kidney disease-related aneurysm.Biochimica et biophysica acta. Molecular cell research · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Converging evidence points to glycogen synthase kinase (GSK) 3 as a key player in the pathogenesis of podocytopathy and proteinuria. However, it remains unclear if GSK3 is involved in podocyte autonomous injury in glomerular disease. In normal kidneys, the β isoform of GSK3 was found to be the major GSK3 expressed in glomeruli and intensely stained in podocytes. GSK3β expression in podocytes was markedly elevated in experimental or human proteinuric glomerulopathy. Podocyte-specific somatic ablation of GSK3β in adult mice attenuated proteinuria and ameliorated podocyte injury and glomerular damage in experimental adriamycin (ADR) nephropathy. Mechanistically, actin cytoskeleton integrity in podocytes was largely preserved in GSK3β knockout mice following ADR insult, concomitant with a correction of podocyte hypermotility and lessened phosphorylation and activation of paxillin, a focal adhesion-associated adaptor protein. In addition, GSK3β knockout diminished ADR-induced NFκB RelA/p65 phosphorylation selectively at serine 467; suppressed de novo expression by podocytes of NFκB-dependent podocytopathic mediators, including B7-1, cathepsin L, and MCP-1; but barely affected the induction of NFκB target pro-survival factors, such as Bcl-xL. Moreover, the ADR-elicited podocytopenia and podocyte death were significantly attenuated in GSK3β knockout mice, associated with protection against podocyte mitochondrial damage and reduced phosphorylation and activation of cyclophilin F, a structural component of mitochondria permeability transition pores. Overall, our findings suggest that the β isoform of GSK3 mediates autonomous podocyte injury in glomerulopathy by integrating multiple podocytopathic signalling pathways.
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Registered trials
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.