ArticleScientific reports2018
Combining streptozotocin and unilateral nephrectomy is an effective method for inducing experimental diabetic nephropathy in the 'resistant' C57Bl/6J mouse strain.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Optimizing diabetic kidney disease animal models: Insights from a meta-analytic approach.Animal models and experimental medicine · 2023Pooled it
- β-Thujaplicin Mobilizes Renal Tubular Iron to Alleviate Diabetic Kidney Disease.Renal failure · 2026Article
- Decreasing S1PR3 Alleviated Renal Tubular Lipid Deposition in Diabetic Nephropathy via AMPK/PPAR-γ/GPAT3 Pathway.Applied biochemistry and biotechnology · 2026Article
- Glomerular Injury Induced by Daily Exposure to the Low-Frequency Component of Environmental Noise via Endothelin Signaling in Mice.Environmental science & technology · 2026Article
- Research and advances in mouse models of diabetic nephropathy: a narrative review.BMC nephrology · 2025Review
- Podocyte-Specific Expression of the Stress Response Protein REDD1 Is Necessary for Diabetes-Induced Podocytopenia.Diabetes · 2025Article
- Construction and evaluation of STZ-induced diabetes and diabetic kidney disease models in C57BL/6J mice.Frontiers in endocrinology · 2025Article
- β-Arrestin-2 enhances endoplasmic reticulum stress-induced glomerular endothelial cell injury by activating transcription factor 6 in diabetic nephropathy.World journal of diabetes · 2024Article
- A novel model of cardiovascular-kidney-metabolic syndrome combining unilateral nephrectomy and high-salt-sugar-fat diet in mice.Lab animal · 2024Article
- Podocyte-specific KLF6 primes proximal tubule CaMK1D signaling to attenuate diabetic kidney disease.Nature communications · 2024Article
- Claudin-2 Mediates the Proximal Tubular Epithelial Cell-Fibroblast Crosstalk via Paracrine CTGF.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- ER Stress-Perturbed Intracellular Protein O-GlcNAcylation Aggravates Podocyte Injury in Diabetes Nephropathy.International journal of molecular sciences · 2023Article
- Effects of Acute and Endurance Exercise on Cerebrovascular Function and Oxygen Metabolism: A Photoacoustic Microscopy Study.IEEE transactions on ultrasonics, ferroelectrics, and frequency control · 2023Article
- Renoprotective Impacts ofInternational journal of molecular sciences · 2023Article
- Bisdemethoxycurcumin Attenuated Renal Injury via Activation of Keap1/Nrf2 Pathway in High-Fat Diet-Fed Mice.International journal of molecular sciences · 2022Article
- High-calorie diet results in reversible obesity-related glomerulopathy in adult zebrafish regardless of dietary fat.American journal of physiology. Renal physiology · 2022Article
- Inhibition of p38 MAPK decreases hyperglycemia-induced nephrin endocytosis and attenuates albuminuria.Journal of molecular medicine (Berlin, Germany) · 2022Article
- TIGAR deficiency sensitizes angiotensin-II-induced renal fibrosis and glomerular injury.Physiological reports · 2022Article
- Liuwei Dihuang Pill Attenuates Diabetic Nephropathy by Inhibiting Renal Fibrosis via TGF-Computational and mathematical methods in medicine · 2022Article
- Streptozotocin-Induced Diabetes in a Mouse Model (BALB/c) Is Not an Effective Model for Research on Transplantation Procedures in the Treatment of Type 1 Diabetes.Biomedicines · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is the leading cause of chronic kidney disease. Animal models are essential tools for designing new strategies to prevent DN. C57Bl/6 (B6) mice are widely used for transgenic mouse models, but are relatively resistant to DN. This study aims to identify the most effective method to induce DN in a type 1 (T1D) and a type 2 diabetes (T2D) model in B6 mice. For T1D-induced DN, mice were fed a control diet, and randomised to streptozotocin (STZ) alone, STZ+unilateral nephrectomy (UNx), or vehicle/sham. For T2D-induced DN, mice were fed a western (high fat) diet, and randomised to either STZ alone, STZ+UNx, UNx alone, or vehicle/sham. Mice subjected to a control diet with STZ +UNx developed albuminuria, glomerular lesions, thickening of the glomerular basement membrane, and tubular injury. Mice on control diet and STZ developed only mild renal lesions. Furthermore, kidneys from mice on a western diet were hardly affected by diabetes, UNx or the combination. We conclude that STZ combined with UNx is the most effective model to induce T1D-induced DN in B6 mice. In our hands, combining western diet and STZ treatment with or without UNx did not result in a T2D-induced DN model in B6 mice.
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