ArticleThe American journal of pathology2014
Glycogen synthase kinase 3β dictates podocyte motility and focal adhesion turnover by modulating paxillin activity: implications for the protective effect of low-dose lithium in podocytopathy.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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47 citing papers in PubMed, 61 citations in OpenAlex.
- Renal glycogen handling in diabetes: A narrative review of diabetic kidney disease pathogenesis.Journal of diabetes investigation · 2026Review
- CLCa mediates a novel cross-talk between Wnt secretion and actin organization.Life science alliance · 2025Article
- Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease.Clinical science (London, England : 1979) · 2025Review
- Integrin Trafficking, Fibronectin Architecture, and Glomerular Injury upon Adiponectin Receptor 1 Depletion.Journal of the American Society of Nephrology : JASN · 2025Article
- Melanocortin 5 receptor signaling protects against podocyte injury in proteinuric glomerulopathies.Kidney international · 2025Article
- CRB2 depletion induces YAP signaling and disrupts mechanosensing in podocytes.American journal of physiology. Renal physiology · 2025Article
- SIRPα modulates the podocyte cytoskeleton through influencing the phosphorylation of FAK at tyrosine residue 597.Acta biochimica et biophysica Sinica · 2024Article
- Genetic deletion of calcium-independent phospholipase A2γ protects mice from diabetic nephropathy.PloS one · 2024Article
- THSD7A-associated membranous nephropathy involves both complement-mediated and autonomous podocyte injury.Frontiers in pharmacology · 2024Article
- Research Progress of Antioxidants in Oxidative Stress Therapy after Spinal Cord Injury.Neurochemical research · 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
- Lithium promotes recovery after spinal cord injury.Neural regeneration research · 2022Article
- Age-related GSK3β overexpression drives podocyte senescence and glomerular aging.The Journal of clinical investigation · 2022Article
- Therapeutic Targeting of GSK3β-Regulated Nrf2 and NFκB Signaling Pathways by Salvianolic Acid A Ameliorates Peritoneal Fibrosis.Frontiers in medicine · 2022Article
- Traditional Chinese Medicine in Treating Primary Podocytosis: From Fundamental Science to Clinical Research.Frontiers in pharmacology · 2022Review
- Cooperation of cell adhesion and autophagy in the brain: Functional roles in development and neurodegenerative disease.Matrix biology plus · 2021Review
- The ketone body β-hydroxybutyrate mitigates the senescence response of glomerular podocytes to diabetic insults.Kidney international · 2021Article
- Safety and Efficacy of Combined Low-Dose Lithium and Low-Dose Aspirin: A Pharmacological and Behavioral Proof-of-Concept Study in Rats.Pharmaceutics · 2021Article
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4 authors at 3 institutions in 2 countries.
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Abstract
Aberrant focal adhesion turnover is centrally involved in podocyte actin cytoskeleton disorganization and foot process effacement. The structural and dynamic integrity of focal adhesions is orchestrated by multiple cell signaling molecules, including glycogen synthase kinase 3β (GSK3β), a multitasking kinase lately identified as a mediator of kidney injury. However, the role of GSK3β in podocytopathy remains obscure. In doxorubicin (Adriamycin)-injured podocytes, lithium, a GSK3β inhibitor and neuroprotective mood stabilizer, obliterated the accelerated focal adhesion turnover, rectified podocyte hypermotility, and restored actin cytoskeleton integrity. Mechanistically, lithium counteracted the doxorubicin-elicited GSK3β overactivity and the hyperphosphorylation and overactivation of paxillin, a focal adhesion-associated adaptor protein. Moreover, forced expression of a dominant negative kinase dead mutant of GSK3β highly mimicked, whereas ectopic expression of a constitutively active GSK3β mutant abolished, the effect of lithium in doxorubicin-injured podocytes, suggesting that the effect of lithium is mediated, at least in part, through inhibition of GSK3β. Furthermore, paxillin interacted with GSK3β and served as its substrate. In mice with doxorubicin nephropathy, a single low dose of lithium ameliorated proteinuria and glomerulosclerosis. Consistently, lithium therapy abrogated GSK3β overactivity, blunted paxillin hyperphosphorylation, and reinstated actin cytoskeleton integrity in glomeruli associated with an early attenuation of podocyte foot process effacement. Thus, GSK3β-modulated focal adhesion dynamics might serve as a novel therapeutic target for podocytopathy.
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