ArticleScientific reports2023
Streptozotocin induces renal proximal tubular injury through p53 signaling activation.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Morphological and Biochemical Insights Into the Renoprotective Effects of Combined N-Acetylcysteine and Glycine Treatment in Experimental Diabetic Nephropathy.Pharmacology research & perspectives · 2026Article
- Animal models for diabetic kidney disease: perspectives and prospects.Frontiers in veterinary science · 2026Article
- TAT-PBX1 Reverses Hyperglycemia Through β-Cell Regeneration and Functional Restoration in an STZ-Induced Diabetic Model.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Protein-bound uremic toxin clearance as biomarker of kidney tubular function in diabetic kidney disease.Scientific reports · 2025Article
- Spinach Extract Reduces Kidney Damage in Diabetic Rats by Impairing the AGEs/RAGE Axis.International journal of molecular sciences · 2025Article
- Early pathological changes in the liver and kidney of non-obese diabetic (NOD) mice: involvement of iron accumulation and ferroptosis.Frontiers in endocrinology · 2025Article
- Knockout of the Carbohydrate Responsive Element Binding Protein Enhances Proliferation and Tumorigenesis in Renal Tubules of Mice.International journal of molecular sciences · 2024Article
- O-GlcNAcylation: Crosstalk between Hemostasis, Inflammation, and Cancer.International journal of molecular sciences · 2024Review
- Chemotherapy-induced acute kidney injury: epidemiology, pathophysiology, and therapeutic approaches.Frontiers in nephrology · 2024Review
- Redox Regulation of Nrf2 in Cisplatin-Induced Kidney Injury.Antioxidants (Basel, Switzerland) · 2023Review
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptozotocin (STZ), an anti-cancer drug that is primarily used to treat neuroendocrine tumors (NETs) in clinical settings, is incorporated into pancreatic β-cells or proximal tubular epithelial cells through the glucose transporter, GLUT2. However, its cytotoxic effects on kidney cells have been underestimated and the underlying mechanisms remain unclear. We herein demonstrated that DNA damage and subsequent p53 signaling were responsible for the development of STZ-induced tubular epithelial injury. We detected tubular epithelial DNA damage in NET patients treated with STZ. Unbiased transcriptomics of STZ-treated tubular epithelial cells in vitro showed the activation of the p53 signaling pathway. STZ induced DNA damage and activated p53 signaling in vivo in a dose-dependent manner, resulting in reduced membrane transporters. The pharmacological inhibition of p53 and sodium-glucose transporter 2 (SGLT2) mitigated STZ-induced epithelial injury. However, the cytotoxic effects of STZ on pancreatic β-cells were preserved in SGLT2 inhibitor-treated mice. The present results demonstrate the proximal tubular-specific cytotoxicity of STZ and the underlying mechanisms in vivo. Since the cytotoxic effects of STZ against β-cells were not impaired by dapagliflozin, pretreatment with an SGLT2 inhibitor has potential as a preventative remedy for kidney injury in NET patients treated with STZ.
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