ArticleScientific reports2018
Comprehensive renoprotective effects of ipragliflozin on early diabetic nephropathy in mice.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 72 citations in OpenAlex.
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- Injured tubule derived CCN1 exacerbates renal congestion-mediated acute kidney injury and fibrosis.Scientific reports · 2025Article
- Implications of Oxidative Stress in the Pathophysiological Pathways of Heart Failure.International journal of molecular sciences · 2025Review
- Unveiling the podocyte-protective effect of sodium-glucose cotransporter-2 inhibitors.Kidney research and clinical practice · 2025Article
- SGLT2i relieve proteinuria in diabetic nephropathy patients potentially by inhibiting renal oxidative stress rather than through AGEs pathway.Diabetology & metabolic syndrome · 2024Article
- The importance of proinflammatory failed-repair tubular epithelia as a predictor of diabetic kidney disease progression.iScience · 2024Article
- Albuminuria and Serum Tumor Necrosis Factor Receptor Levels in Patients with Type 2 Diabetes on SGLT2 Inhibitors: A Prospective Study.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2024Article
- Mechanisms of enhanced renal and hepatic erythropoietin synthesis by sodium-glucose cotransporter 2 inhibitors.European heart journal · 2023Article
- Galantamine improves glycemic control and diabetic nephropathy in LeprScientific reports · 2023Article
- Redox regulation in diabetic kidney disease.American journal of physiology. Renal physiology · 2023Review
- Nephroprotective Effects of Dapagliflozin in Patients with Type 2 Diabetes.Internal medicine (Tokyo, Japan) · 2023Article
- SGLT2 inhibitors, intrarenal hypoxia and the diabetic kidney: insights into pathophysiological concepts and current evidence.Archives of medical sciences. Atherosclerotic diseases · 2023Article
- Tubular injury in diabetic kidney disease: molecular mechanisms and potential therapeutic perspectives.Frontiers in endocrinology · 2023Review
- Enhanced Cardiorenal Protective Effects of Combining SGLT2 Inhibition, Endothelin Receptor Antagonism and RAS Blockade in Type 2 Diabetic Mice.International journal of molecular sciences · 2022Article
- Exploring molecular targets in diabetic kidney disease.Kidney research and clinical practice · 2022Article
- Proximal tubular epithelia-specific transcriptomics of diabetic mice treated with dapagliflozin.Heliyon · 2022Article
- Article
- "Greedy Organs Hypothesis" for sugar and salt in the pathophysiology of non-communicable diseases in relation to sodium-glucose co-transporters in the intestines and the kidney.Metabolism open · 2022Review
- Direct evidence of proximal tubular proliferation in early diabetic nephropathy.Scientific reports · 2022Article
- Antioxidant Roles of SGLT2 Inhibitors in the Kidney.Biomolecules · 2022Review
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinical and experimental studies have shown that sodium glucose co-transporter 2 inhibitors (SGLT2i) contribute to the prevention of diabetic kidney disease progression. In order to clarify its pharmacological effects on the molecular mechanisms underlying the development of diabetic kidney disease, we administered different doses of the SGLT2i, ipragliflozin, to type 2 diabetic mice. A high-dose ipragliflozin treatment for 8 weeks lowered blood glucose levels and reduced urinary albumin excretion. High- and low-dose ipragliflozin both inhibited renal and glomerular hypertrophy, and reduced NADPH oxidase 4 expression and subsequent oxidative stress. Analysis of glomerular phenotypes using glomeruli isolation demonstrated that ipragliflozin preserved podocyte integrity and reduced oxidative stress. Regarding renal tissue hypoxia, a short-term ipragliflozin treatment improved oxygen tension in the kidney cortex, in which SGLT2 is predominantly expressed. We then administered ipragliflozin to type 1 diabetic mice and found that high- and low-dose ipragliflozin both reduced urinary albumin excretion. In conclusion, we confirmed dose-dependent differences in the effects of ipragliflozin on early diabetic nephropathy in vivo. Even low-dose ipragliflozin reduced renal cortical hypoxia and abnormal hemodynamics in early diabetic nephropathy. In addition to these effects, high-dose ipragliflozin exerted renoprotective effects by reducing oxidative stress in tubular epithelia and glomerular podocytes.
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