ArticleScientific reports2025
Dapagliflozin inhibits ferroptosis and ameliorates renal fibrosis in diabetic C57BL/6J mice.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Dapagliflozin attenuates ferroptosis in diabetic nephropathy through activation of the Nrf2/HO‑1 signaling pathway.International journal of molecular medicine · 2026Article
- Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Advances in targeted treatment of ferroptosis in diabetic kidney disease with SGLT2 inhibitors.Diabetology & metabolic syndrome · 2026Review
- Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Beneficial Effects of Sodium-Glucose Cotransporter 2 Inhibitors in Cisplatin Nephrotoxicity: A Mechanistic Review.Kidney360 · 2026Review
- Renoprotective effects of SGLT2 inhibitors in patients with Fabry disease.Molecular genetics and metabolism reports · 2025Article
- Non-Coding RNA in Type 2 Diabetes Cardio-Renal Complications and SGLT2 Inhibitor Response.International journal of molecular sciences · 2025Review
- Ferroptosis and pyroptosis in diabetes mellitus: emerging therapeutic potential of GLP-1 receptor agonists.Frontiers in clinical diabetes and healthcare · 2025Review
- Targeting ion channel networks in diabetic kidney disease: from molecular crosstalk to precision therapeutics and clinical innovation.Frontiers in medicine · 2025Review
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9 authors.
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Abstract
Diabetic nephropathy (DN) is a common complication of diabetes and a major cause of end-stage renal disease, with complex pathogenesis involving inflammation, oxidative stress, fibrosis, and ferroptosis. Ferroptosis is linked to DN progression, yet treatment options are limited, particularly for targeting ferroptosis. Dapagliflozin (DAPA), an SGLT2 inhibitor, shows renal protective effects in diabetes, but its role in renal fibrosis and ferroptosis in DN is unclear. This study investigated DAPA's effect on renal fibrosis in DN by inhibiting ferroptosis, using a streptozotocin-induced diabetic mouse model. Results indicated that DAPA improved renal function, reduced fibrosis, and suppressed ferroptosis markers in diabetic mice. In vitro, DAPA inhibited ferroptosis and fibrosis in HK-2 cells under high glucose conditions. Molecular docking and network pharmacology suggested DAPA's anti-fibrotic and anti-ferroptotic effects may involve the Nrf2 and TGF-β signaling pathways. DAPA also reduced serum creatinine and blood urea nitrogen in diabetic mice, improved glomerulosclerosis and interstitial fibrosis, decreased iron deposition, and enhanced antioxidant activity. Overall, DAPA's multi-target mechanisms significantly improve DN progression, suggesting its potential as a targeted therapy against ferroptosis. Future studies should further explore DAPA's applications.
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