ArticlePharmacology research & perspectives2016
Inhibition of SGLT2 alleviates diabetic nephropathy by suppressing high glucose-induced oxidative stress in type 1 diabetic mice.
Article in Pharmacology research & perspectives, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Effect of Insulin on Proximal Tubules Handling of Glucose: A Systematic Review.Journal of diabetes research · 2020Pooled it
- Tubular injury in diabetic kidney disease: a focus on regulated cell death.Frontiers in endocrinology · 2026Review
- Combined dapagliflozin and pioglitazone therapy in diabetic nephropathy: no added benefit beyond monotherapy in inflammation and fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Chronic cardiorenal syndrome: cardio-renal protective effect of SGLT2i.Renal failure · 2025Review
- Sodium-Glucose Cotransporter-2 Inhibitor Improves Renal Injury by Regulating the Redox Profile, Inflammatory Parameters, and Pyroptosis in an Experimental Model of Diabetic Kidney Disease.ACS pharmacology & translational science · 2025Article
- Combination of dapagliflozin and pioglitazone lacks superiority against monotherapy in streptozotocin-induced nephropathy.Scientific reports · 2025Article
- Proximal tubule hypertrophy and hyperfunction: a novel pathophysiological feature in disease states.Clinical kidney journal · 2024Review
- The Renoprotective Mechanisms of Sodium-Glucose Cotransporter-2 Inhibitors (SGLT2i)-A Narrative Review.International journal of molecular sciences · 2024Review
- Dapagliflozin mitigates oxidative stress, inflammatory, and histopathological markers of aging in mice.Journal of medicine and life · 2024Article
- Association between different insulin resistance indices and all-cause mortality in patients with diabetic kidney disease: a prospective cohort study.Frontiers in endocrinology · 2024Article
- Combination of canagliflozin and puerarin alleviates the lipotoxicity to diabetic kidney in mice.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- Transcription factor c-Maf deletion improves streptozotocin-induced diabetic nephropathy by directly regulating Sglt2 and Glut2.JCI insight · 2023Article
- The Mitochondrion: A Promising Target for Kidney Disease.Pharmaceutics · 2023Review
- Possible renoprotective mechanisms of SGLT2 inhibitors.Frontiers in medicine · 2023Review
- Liraglutide Attenuates Hepatic Oxidative Stress, Inflammation, and Apoptosis in Streptozotocin-Induced Diabetic Mice by Modulating the Wnt/Mediators of inflammation · 2023Article
- Dapagliflozin Prevents High-Glucose-Induced Cellular Senescence in Renal Tubular Epithelial Cells.International journal of molecular sciences · 2022Article
- Biomolecular Mechanisms of Cardiorenal Protection with Sodium-Glucose Co-Transporter 2 Inhibitors.Biomolecules · 2022Review
- Reprogramming Metabolism of Macrophages as a Target for Kidney Dysfunction Treatment in Autoimmune Diseases.International journal of molecular sciences · 2022Review
- Role of Sodium-Glucose Co-Transporter 2 Inhibitors in the Regulation of Inflammatory Processes in Animal Models.International journal of molecular sciences · 2022Review
- Effects of the SGLT2 Inhibition on Cardiac Remodeling in Streptozotocin-Induced Diabetic Rats, a Model of Type 1 Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2022Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is unclear whether the improvement in diabetic nephropathy by sodium glucose cotransporter 2 (SGLT2) inhibitors is caused by a direct effect on SGLT2 or by the improvement in hyperglycemia. Here, we investigated the effect of dapagliflozin on early-stage diabetic nephropathy using a mouse model of type 1 diabetes and murine proximal tubular epithelial cells. Eight-week-old Akita mice were treated with dapagliflozin or insulin for 12 weeks. Body weight, urinary albumin excretion, blood pressure, as well as levels of blood glucose and hemoglobin A1c were measured. Expansion of the mesangial matrix, interstitial fibrosis, and macrophage infiltration in kidneys were evaluated by histology. Oxidative stress and apoptosis were evaluated in kidneys and cultured proximal tubular epithelial cells. Compared with nontreated mice, dapagliflozin and insulin decreased blood glucose and hemoglobin A1c levels equally. Urine volume and water intake increased significantly in the dapagliflozin-treated group compared with those in the insulin-treated group, but there were no differences in body weight or blood pressure between the two groups. Macrophage infiltration and fibrosis in renal interstitium improved significantly in the dapagliflozin group compared with the insulin group. Oxidative stress was attenuated by dapagliflozin, and suppression occurred in a dose-dependent manner. RNAi knockdown of SGLT2 resulted in reduced oxidative stress. Dapagliflozin ameliorates diabetic nephropathy by suppressing hyperglycemia-induced oxidative stress in a manner independent of hyperglycemia improvement in Akita mice. Our findings suggest that dapagliflozin may be a novel therapeutic approach for the treatment of diabetic nephropathy.
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