ArticleNature communications2019
Podocyte GSK3 is an evolutionarily conserved critical regulator of kidney function.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 71 citations in OpenAlex.
- The insulin/IGF axis is critically important for controlling gene transcription in the podocyte.eLife · 2026Article
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- The IQGAP1-claudin cell junction axis in cisplatin-induced epithelial damage.Cell communication and signaling : CCS · 2026Article
- Signal Transducer and Activator of Transcription 3 in the Podocyte: A Key Mediator of Podocyte-Parietal Epithelial Cell Cross-Talk and Glomerular Health?Journal of the American Society of Nephrology : JASN · 2026Article
- Lithium-induced kidney injury and fibrosis: A versatile model to explore cellular pathways of injury and repair.Physiological reports · 2025Review
- Podocyte YAP and TAZ hyperactivation drives glomerular epithelial proliferative diseases in mice and humans.Science translational medicine · 2025Article
- Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease.Clinical science (London, England : 1979) · 2025Review
- Liposome-Polymer Nanoparticles Loaded with Copper Diethyldithiocarbamate and 6-Bromo-Indirubin-3'-Oxime Enable the Treatment of Refractive Melanoma.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Brown adipose tissue alleviates podocyte apoptosis through NRG4 in a male mouse model of diabetic kidney disease.Diabetologia · 2025Article
- Cell cycle disorders in podocytes: an emerging and increasingly recognized phenomenon.Cell death discovery · 2025Review
- Piezo1, F-Actin Remodeling, and Podocyte Survival and Regeneration.Journal of the American Society of Nephrology : JASN · 2025Article
- LncRNA evf-2 Exacerbates Podocyte Injury in Diabetic Nephropathy by Inducing Cell Cycle Re-entry and Inflammation Through Distinct Mechanisms Triggered by hnRNPU.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The state of the art in secondary pharmacology and its impact on the safety of new medicines.Nature reviews. Drug discovery · 2024Review
- Contrasting consequences of podocyte insulin-like growth factor 1 receptor inhibition.iScience · 2024Article
- Insights into human kidney function from the study of Drosophila.Pediatric nephrology (Berlin, Germany) · 2023Review
- Review
- Phosphoproteome Profiling of uEVs Reveals p-AQP2 and p-GSK3β as Potential Markers for Diabetic Nephropathy.Molecules (Basel, Switzerland) · 2023Article
- Recent Advances in Proteinuric Kidney Disease/Nephrotic Syndrome: Lessons from Knockout/Transgenic Mouse Models.Biomedicines · 2023Review
- AZD5438 a GSK-3a/b and CDK inhibitor is antiapoptotic modulates mitochondrial activity and protects human neurons from mitochondrial toxins.Scientific reports · 2023Article
- Long non-coding RNA DLX6-AS1 is the key mediator of glomerular podocyte injury and albuminuria in diabetic nephropathy by targeting the miR-346/GSK-3β signaling pathway.Cell death & disease · 2023Article
Corrections and comments
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Authors and funding
23 authors at 7 institutions in 5 countries.
Funding
Abstract
Albuminuria affects millions of people, and is an independent risk factor for kidney failure, cardiovascular morbidity and death. The key cell that prevents albuminuria is the terminally differentiated glomerular podocyte. Here we report the evolutionary importance of the enzyme Glycogen Synthase Kinase 3 (GSK3) for maintaining podocyte function in mice and the equivalent nephrocyte cell in Drosophila. Developmental deletion of both GSK3 isoforms (α and β) in murine podocytes causes late neonatal death associated with massive albuminuria and renal failure. Similarly, silencing GSK3 in nephrocytes is developmentally lethal for this cell. Mature genetic or pharmacological podocyte/nephrocyte GSK3 inhibition is also detrimental; producing albuminuric kidney disease in mice and nephrocyte depletion in Drosophila. Mechanistically, GSK3 loss causes differentiated podocytes to re-enter the cell cycle and undergo mitotic catastrophe, modulated via the Hippo pathway but independent of Wnt-β-catenin. This work clearly identifies GSK3 as a critical regulator of podocyte and hence kidney function.
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