ArticleKidney international2015
Fine-tuning of NFκB by glycogen synthase kinase 3β directs the fate of glomerular podocytes upon injury.
Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- Disruptions of cell signaling pathways in myotonic dystrophy type 1 skeletal muscle, their pathogenic impact, and potential for combinatorial therapeutics.The Journal of biological chemistry · 2026Review
- Intercepting the complement amplification loop through podocyte MC5R signaling ameliorates membranous nephropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease.Clinical science (London, England : 1979) · 2025Review
- Melanocortin 5 receptor signaling protects against podocyte injury in proteinuric glomerulopathies.Kidney international · 2025Article
- A Small Molecule Agonist of Krüppel-Like Factor 15 in Proteinuric Kidney Disease.Journal of the American Society of Nephrology : JASN · 2024Article
- A simple protocol to establish a conditionally immortalized mouse podocyte cell line.Scientific reports · 2024Article
- Lithium-induced apoptotic cell death is not accompanied by a noticeable inflammatory response in the kidney.Frontiers in physiology · 2024Article
- Piperazine ferulate inhibits diabetic nephropathy by suppressing AGE/RAGE-mediated inflammatory signaling in rats and podocytes.Frontiers in pharmacology · 2024Article
- THSD7A-associated membranous nephropathy involves both complement-mediated and autonomous podocyte injury.Frontiers in pharmacology · 2024Article
- From Physiology to Pathology: The Role of Mitochondria in Acute Kidney Injuries and Chronic Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2023Review
- Dietary lithium intake, graft failure and mortality in kidney transplant recipients.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023Article
- TYRO3 agonist as therapy for glomerular disease.JCI insight · 2023Article
- Angiotensin II type-2-receptor stimulation ameliorates focal and segmental glomerulosclerosis in mice.Clinical science (London, England : 1979) · 2022Article
- Pharmacological Melanocortin 5 Receptor Activation Attenuates Glomerular Injury and Proteinuria in Rats With Puromycin Aminonucleoside Nephrosis.Frontiers in physiology · 2022Article
- Traditional Chinese Medicine in Treating Primary Podocytosis: From Fundamental Science to Clinical Research.Frontiers in pharmacology · 2022Review
- Therapeutic Targeting of GSK3β-Regulated Nrf2 and NFκB Signaling Pathways by Salvianolic Acid A Ameliorates Peritoneal Fibrosis.Frontiers in medicine · 2022Article
- Safety and Efficacy of Combined Low-Dose Lithium and Low-Dose Aspirin: A Pharmacological and Behavioral Proof-of-Concept Study in Rats.Pharmaceutics · 2021Article
- Relationship between lysosomal dyshomeostasis and progression of diabetic kidney disease.Cell death & disease · 2021Review
- Permissive effect of GSK3β on profibrogenic plasticity of renal tubular cells in progressive chronic kidney disease.Cell death & disease · 2021Article
- The protective effect of beta-hydroxybutyric acid on renal glomerular epithelial cells in adriamycin-induced injury.American journal of translational research · 2021Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) is regulated by a myriad of signaling cascades including glycogen synthase kinase (GSK) 3β and plays a Janus role in podocyte injury. In vitro, lipopolysaccharide (LPS) or adriamycin (ADR) elicited podocyte injury and cytoskeletal disruption, associated with NFκB activation and induced expression of NFκB target molecules, including pro-survival Bcl-xL and podocytopathic mediators like MCP-1, cathepsin L, and B7-1. Broad-range inhibition of NFκB diminished the expression of all NFκB target genes, restored cytoskeleton integrity, but potentiated apoptosis. In contrast, blockade of GSK3β by lithium or 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8) mitigated the expression of podocytopathic mediators, ameliorated podocyte injury, but barely affected Bcl-xL expression or sensitized apoptosis. Mechanistically, GSK3β was sufficient and essential for RelA/p65 phosphorylation, specifically at serine 467, which specifies the expression of selective NFκB target molecules, including podocytopathic mediators, but not Bcl-xL. In vivo, lithium or TDZD-8 therapy improved podocyte injury and proteinuria in mice treated with LPS or ADR, concomitant with the suppression of podocytopathic mediators, but retained Bcl-xL in glomerulus. Broad-range inhibition of NFκB conferred similar but much weakened antiproteinuric and podoprotective effects accompanied with a blunted glomerular expression of Bcl-xL and marked podocyte apoptosis. Thus, the GSK3β-dictated fine-tuning of NFκB may serve as a novel therapeutic target for podocytopathy.
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Registered trials
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