ArticleThe Journal of biological chemistry2014
Activation of glycogen synthase kinase 3β ameliorates diabetes-induced kidney injury.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 47 citations in OpenAlex.
- Renal glycogen handling in diabetes: A narrative review of diabetic kidney disease pathogenesis.Journal of diabetes investigation · 2026Review
- Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease.Clinical science (London, England : 1979) · 2025Review
- High glucose couples DJ-1 with PTEN to activate PDGFRβ for renal proximal tubular cell injury.PloS one · 2025Article
- Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Phosphoproteome Profiling of uEVs Reveals p-AQP2 and p-GSK3β as Potential Markers for Diabetic Nephropathy.Molecules (Basel, Switzerland) · 2023Article
- β-RA Targets Mitochondrial Metabolism and Adipogenesis, Leading to Therapeutic Benefits against CoQ Deficiency and Age-Related Overweight.Biomedicines · 2021Article
- Review
- Proximal tubular epithelial insulin receptor mediates high-fat diet-induced kidney injury.JCI insight · 2021Article
- Geniposide Improves Diabetic Nephropathy by Enhancing ULK1-Mediated Autophagy and Reducing Oxidative Stress through AMPK Activation.International journal of molecular sciences · 2021Article
- Mechanisms of Herbal Nephroprotection in diabetes mellitus.Journal of diabetes research · 2020Review
- Glucose and glycogen in the diabetic kidney: Heroes or villains?EBioMedicine · 2019Review
- Overexpression of Circulating Soluble Nogo-B Improves Diabetic Kidney Disease by Protecting the Vasculature.Diabetes · 2019Article
- Marmoset as a Model to Study Kidney Changes Associated With Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2019Article
- High glucose reduces megalin-mediated albumin endocytosis in renal proximal tubule cells through protein kinase BThe Journal of biological chemistry · 2018Article
- Lack of serum- and glucocorticoid-inducible kinase 3 leads to podocyte dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- tRNA fragmentation and protein translation dynamics in the course of kidney injury.RNA biology · 2018Review
- Surprising Enhancement of Fibrosis by Tubule-Specific Deletion of the TGF-Journal of the American Society of Nephrology : JASN · 2017Article
- Renoprotective effects of emodin against diabetic nephropathy in rat models are mediated via PI3K/Akt/GSK-3β and Bax/caspase-3 signaling pathways.Experimental and therapeutic medicine · 2017Article
- Rescue therapy with Tanshinone IIA hinders transition of acute kidney injury to chronic kidney disease via targeting GSK3β.Scientific reports · 2016Article
- Glycogen synthase kinase‑3β is required for epithelial‑mesenchymal transition and barrier dysfunction in mouse podocytes under high glucose conditions.Molecular medicine reports · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Increase in protein synthesis contributes to kidney hypertrophy and matrix protein accumulation in diabetes. We have previously shown that high glucose-induced matrix protein synthesis is associated with inactivation of glycogen synthase kinase 3β (GSK3β) in renal cells and in the kidneys of diabetic mice. We tested whether activation of GSK3β by sodium nitroprusside (SNP) mitigates kidney injury in diabetes. Studies in kidney-proximal tubular epithelial cells showed that SNP abrogated high glucose-induced laminin increment by stimulating GSK3β and inhibiting Akt, mTORC1, and events in mRNA translation regulated by mTORC1 and ERK. NONOate, an NO donor, also activated GSK3β, indicating that NO may mediate SNP stimulation of GSK3β. SNP administered for 3 weeks to mice with streptozotocin-induced type 1 diabetes ameliorated kidney hypertrophy, accumulation of matrix proteins, and albuminuria without changing blood glucose levels. Signaling studies showed that diabetes caused inactivation of GSK3β by activation of Src, Pyk2, Akt, and ERK; GSK3β inhibition activated mTORC1 and downstream events in mRNA translation in the kidney cortex. These reactions were abrogated by SNP. We conclude that activation of GSK3β by SNP ameliorates kidney injury induced by diabetes.
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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.