ArticleScientific reports2019
Amelioration of diabetic nephropathy by SGLT2 inhibitors independent of its glucose-lowering effect: A possible role of SGLT2 in mesangial cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 75 citations in OpenAlex.
- A metabolomics-based molecular pathway analysis of how the sodium-glucose co-transporter-2 inhibitor dapagliflozin may slow kidney function decline in patients with diabetes.Diabetes, obesity & metabolism · 2020 · on this mapTrial
- Mogroside V Alleviates Renal Injury in Diabetic Mice via Regulation of theInternational journal of molecular sciences · 2026Article
- Advances in targeted treatment of ferroptosis in diabetic kidney disease with SGLT2 inhibitors.Diabetology & metabolic syndrome · 2026Review
- Molecular Mechanisms and Clinical Evidence Supporting the Four Pillars of Therapy in Diabetic Kidney Disease: Emerging Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- mTOR blockade prevents progressive proteinuria but induces hyperglycaemia in obese Dahl salt-sensitive rats before puberty.Experimental physiology · 2025Article
- Effect of Anti-Diabetic Medication Use on Sepsis Risk in Type 2 Diabetes Mellitus: A Multivariate Analysis.Geriatrics (Basel, Switzerland) · 2025Article
- Antioxidant Effects of SGLT2 Inhibitors on Cardiovascular-Kidney-Metabolic (CKM) Syndrome.Antioxidants (Basel, Switzerland) · 2025Review
- Mizagliflozin ameliorates diabetes induced kidney injury by inhibitor inhibit inflammation and oxidative stress.World journal of diabetes · 2025Article
- Sodium glucose co-transporter 2 inhibitors (SGLT2i) for pediatric kidney disease: the future is near.Frontiers in pediatrics · 2025Review
- Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications.International journal of biological sciences · 2025Review
- SGLT2 inhibition mitigates transition from acute kidney injury to chronic kidney disease by suppressing ferroptosis.Scientific reports · 2024Article
- The Early Pathogenesis of Diabetic Retinopathy and Its Attenuation by Sodium-Glucose Transporter 2 Inhibitors.Diabetes · 2024Article
- Potentials of Natural Antioxidants in Reducing Inflammation and Oxidative Stress in Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- SGLT2 Inhibitor Canagliflozin Alleviates High Glucose-Induced Inflammatory Toxicity in BV-2 Microglia.Biomedicines · 2023Article
- Redox regulation in diabetic kidney disease.American journal of physiology. Renal physiology · 2023Review
- Cellular interplay between cardiomyocytes and non-myocytes in diabetic cardiomyopathy.Cardiovascular research · 2023Review
- Article
- Nephroprotective Effects of Dapagliflozin in Patients with Type 2 Diabetes.Internal medicine (Tokyo, Japan) · 2023Article
- SGLT-2 inhibitors in nephrotic-range proteinuria: emerging clinical evidence.Clinical kidney journal · 2023Review
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Authors and funding
8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Several clinical studies have shown the beneficial effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors on diabetic nephropathy. The underlying mechanisms are not fully understood. We found that administration of canagliflozin at a low dose (0.01 mg/kg/day) did not affect either blood glucose levels or glycosuria, but it improved albuminuria and mesangial expansion in db/db mice to a similar extent as at a high dose (3.0 mg/kg/day) that lowered blood glucose levels. This indicated the existence of a tubular SGLT2-independent reno-protective mechanism. Here we focused on the potential role of SGLT2 in mesangial cells (MCs). Western blot analysis revealed the expression of SGLT2 in cultured mouse MCs. Exposure of MCs to high glucose levels for 72 h significantly increased the expression of SGLT2. Canagliflozin or ipragliflozin (both 100 nM) treatment inhibited glucose consumption in the medium under high-glucose conditions but not under normal-glucose conditions. Furthermore, canagliflozin inhibited high-glucose-induced activation of the protein kinase C (PKC)-NAD(P)H oxidase pathway and increases in reactive oxygen species (ROS) production. Thus, the inhibition of mesangial SGLT2 may cause an inhibition of PKC activation and ROS overproduction in diabetic nephropathy, and this may at least in part account for the reno-protective effect of SGLT2 inhibitors.
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