ArticleThe Journal of pathology2015
Loss of PTEN promotes podocyte cytoskeletal rearrangement, aggravating diabetic nephropathy.
Article in The Journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 67 citations in OpenAlex.
- PTEN modulates mitochondrial dysfunction in podocytes via the PINK1/Parkin signal pathway.Translational pediatrics · 2026Article
- Experimental Validation and Bioinformatics Analysis Elucidate the Role of MTDH-Mediated PTEN Ubiquitination and Degradation in Podocyte Injury in Diabetic Kidney Disease.Human mutation · 2026Article
- Therapeutic Effect of Lebanese Cannabis Oil Extract in the Management of Sodium Orthovanadate-Induced Nephrotoxicity in Rats.International journal of molecular sciences · 2025Article
- Ferulic acid lipid nano capsules versus its native form in alleviating diabetic nephropathy induced in rats through TGF-β1/Hippo pathway crosstalk modulation.Scientific reports · 2025Article
- PTEN: A Novel Diabetes Nephropathy Protective Gene Related to Cellular Senescence.International journal of molecular sciences · 2025Article
- Therapeutic potential of exosomal lncRNAs derived from stem cells in wound healing: focusing on mesenchymal stem cells.Stem cell research & therapy · 2025Review
- Amine-Functionalized Gellan Gum-Based Hydrogel Loaded with Adipose Stem Cell-Derived Small Extracellular Vesicles: An In Vitro Proof of Concept for Enhancing Diabetic Foot Ulcer Healing.Gels (Basel, Switzerland) · 2025Article
- Spatiotemporal distribution of PTEN before directed cell migration in monolayers.In vitro cellular & developmental biology. Animal · 2024Article
- Analysis of an adult diabetes mellitus caused by a rare mutation of the gene: A case report.World journal of clinical cases · 2024Article
- Cell division cycle 42 attenuates high glucose-treated renal tubular epithelial cell apoptosis, fibrosis, and inflammation, but activates the PAK1/AKT pathway.Clinical and experimental nephrology · 2024Article
- Urinary Excretion of Biomolecules Related to Cell Cycle, Proliferation, and Autophagy in Subjects with Type 2 Diabetes and Chronic Kidney Disease.Biomedicines · 2024Article
- Recent Advances in Proteinuric Kidney Disease/Nephrotic Syndrome: Lessons from Knockout/Transgenic Mouse Models.Biomedicines · 2023Review
- Loss of Pten in Renal Tubular Cells Leads to Water Retention by Upregulating AQP2.Kidney diseases (Basel, Switzerland) · 2023Article
- Urinary-derived extracellular vesicles reveal a distinct microRNA signature associated with the development and progression of Fabry nephropathy.Frontiers in medicine · 2023Article
- Transcriptome expression profiles associated with diabetic nephropathy development.Molecular and cellular biochemistry · 2022Article
- PI(4,5)P2 controls slit diaphragm formation and endocytosis in Drosophila nephrocytes.Cellular and molecular life sciences : CMLS · 2022Article
- Serum Level of Polyubiquitinated PTEN and Loss of Kidney Function in American Indians With Type 2 Diabetes.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2022Observational
- Rho GTPases in kidney physiology and diseases.Small GTPases · 2022Article
- NLRP3-mediated pyroptosis in diabetic nephropathy.Frontiers in pharmacology · 2022Review
- The role of PTEN in puromycin aminonucleoside-induced podocyte injury.International journal of medical sciences · 2022Article
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
In diabetic nephropathy (DN), podocyte cytoskeletal rearrangement occurs followed by podocyte effacement and the development of proteinuria. PTEN (phosphatase and tensin homologue) is a ubiquitously expressed phosphatase that plays a critical role in cell proliferation, cytoskeletal rearrangement, and motility. In mouse models of diabetes mellitus, PTEN expression is reportedly decreased in mesangial cells, contributing to expansion of the mesangial matrix, but how PTEN in the podocyte influences the development of DN is unknown. We observed that PTEN expression is down-regulated in the podocytes of diabetic db/db mice and patients with DN. In cultured podocytes, PTEN inhibition caused actin cytoskeletal rearrangement and this response was associated with unbalanced activation of the small GTPases Rac1/Cdc42 and RhoA. In mice treated with PTEN inhibitor, actin cytoskeletal rearrangement occurred in podocytes and was accompanied by increased albumin excretion. We also created mice with an inducible deletion of PTEN selectively in podocytes. These mice exhibited increased albumin excretion and moderate foot process effacement. When the mice were challenged with a high fat diet, podocyte-specific knockout of PTEN resulted in substantially increased proteinuria and glomeruloclerosis compared to control mice fed a high fat diet or mice with PTEN deletion fed a normal diet. These results indicate that PTEN is involved in the regulation of cytoskeletal rearrangement in podocytes and that loss of PTEN predisposes to the development of proteinuria and DN.
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