ArticleBiomolecules2020
SGLT2 Inhibition by Intraperitoneal Dapagliflozin Mitigates Peritoneal Fibrosis and Ultrafiltration Failure in a Mouse Model of Chronic Peritoneal Exposure to High-Glucose Dialysate.
Article in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 66 citations in OpenAlex.
- SGLT2 inhibitors attenuate nephrin loss and enhance TGF-βScientific reports · 2022Trial
- SGLT2 inhibitors in hemodialysis or peritoneal dialysis patients: rationale and state-of-the art.Clinical kidney journal · 2026Review
- SGLT2 inhibitors as a strategy for volume management in peritoneal dialysis: a case series.Frontiers in nephrology · 2026Article
- Empagliflozin and Ultrafiltration Volume in Patients Undergoing Peritoneal Dialysis.Kidney international reports · 2026Article
- Dapagliflozin ameliorates high glucose-induced peritoneal fibrosis through downregulation of ENKUR/PI3K/AKT signaling pathway.Scientific reports · 2025Article
- Nicotinamide nucleotide transhydrogenase deficiency and genetic susceptibility to high glucose-mediated peritoneal injury in mice.Physiological reports · 2025Article
- Glycemic Control in Patients with Diabetes on Peritoneal Dialysis: From Glucose Sparing Approach to Glucose Monitoring.Life (Basel, Switzerland) · 2025Review
- Anti-Inflammatory Effects of SGLT2 Inhibitors: Focus on Macrophages.International journal of molecular sciences · 2025Review
- Molecular and Functional Characterization of the Peritoneal Mesothelium, a Barrier for Solute Transport.Function (Oxford, England) · 2025Article
- Dose-Response Relationship of Phloretin Therapy on Water and Glucose Transport during Experimental Peritoneal Dialysis.Kidney360 · 2025Article
- Peritoneal Dialysis -Associated Fibrosis: Emerging Mechanisms and Therapeutic Opportunities.Frontiers in pharmacology · 2025Review
- Benefits of SGLT2 inhibitors in patients with diabetes and advanced chronic kidney disease - where have we gone so far?Frontiers in clinical diabetes and healthcare · 2025Review
- SGLT-2 inhibitors in chronic peritoneal dialysis patients: a follow-up study.BMC nephrology · 2024Observational
- Effects of Sodium-Glucose Cotransporter 2 Inhibitors in Diabetic and Non-Diabetic Patients with Advanced Chronic Kidney Disease in Peritoneal Dialysis on Residual Kidney Function: In Real-World Data.Medicina (Kaunas, Lithuania) · 2024Observational
- Effects of sodium-glucose co-transporter 2 inhibitors on ultrafiltration in patients with peritoneal dialysis: a protocol for a randomized, double-blind, placebo-controlled, crossover trial (EMPOWERED).Clinical and experimental nephrology · 2024Article
- Research advances in the anti-inflammatory effects of SGLT inhibitors in type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2024Review
- Review
- Coupling Osmotic Efficacy with Biocompatibility in Peritoneal Dialysis: A Stiff Challenge.International journal of molecular sciences · 2024Review
- Integrative analysis of chromatin accessibility and transcriptome landscapes in the induction of peritoneal fibrosis by high glucose.Journal of translational medicine · 2024Article
- Dapagliflozin in peritoneal dialysis patients: a pilot study evaluating peritoneal membrane function.BMC nephrology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Peritoneal dialysis (PD) is limited by glucose-mediated peritoneal membrane (PM) fibrosis, angiogenesis, and ultrafiltration failure. Influencing PM integrity by pharmacologically targeting sodium-dependent glucose transporter (SGLT)-mediated glucose uptake has not been studied. In this study, wildtype C57Bl/6N mice were treated with high-glucose dialysate via an intraperitoneal catheter, with or without addition of selective SGLT2 inhibitor dapagliflozin. PM structural changes, ultrafiltration capacity, and peritoneal equilibration testing (PET) status for glucose, urea, and creatinine were analyzed. Expression of SGLT and facilitative glucose transporters (GLUT) was analyzed by real-time PCR, immunofluorescence, and immunohistochemistry. Peritoneal effluents were analyzed for cellular and cytokine composition. We found that peritoneal SGLT2 was expressed in mesothelial cells and in skeletal muscle. Dapagliflozin significantly reduced effluent transforming growth factor (TGF-β) concentrations, peritoneal thickening, and fibrosis, as well as microvessel density, resulting in improved ultrafiltration, despite the fact that it did not affect development of high-glucose transporter status. In vitro, dapagliflozin reduced monocyte chemoattractant protein-1 release under high-glucose conditions in human and murine peritoneal mesothelial cells. Proinflammatory cytokine release in macrophages was reduced only when cultured in high-glucose conditions with an additional inflammatory stimulus. In summary, dapagliflozin improved structural and functional peritoneal health in the context of high-glucose PD.
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