ArticleKidney3602026
Dapagliflozin Reduces Kidney Inflammation in Alport Syndrome by Inhibiting the Stimulator of IFN Genes Pathway in Renal Tubular Epithelial Cells.
Article in Kidney360, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Renal Tubular Epithelial Cells as Central Hubs of Kidney Disease.Diagnostics (Basel, Switzerland) · 2026Review
- Sodium-Glucose Cotransporter 2 Inhibitors in Alport Syndrome: Emerging Clinical Evidence and Mechanistic Insights.Kidney360 · 2026Article
- Dapagliflozin Augmentation of Sacubitril/Valsartan Therapy in Patients With Heart Failure Following PCI-Treated Acute Myocardial Infarction: A Meta-Analysis of Clinical Efficacy and Safety.Cardiology research and practice · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
key pointsDapagliflozin reduces proteinuria in patients with Alport syndrome. Dapagliflozin plays an anti-inflammatory role by inhibiting the stimulator of IFN genes pathway in tubular epithelial cells of Alport syndrome mice.
backgroundAlport syndrome (AS) is a hereditary kidney disease caused by COL4A3/4/5 mutations that lack of effective treatments. Sodium-glucose cotransporter 2 inhibitors have demonstrated renal and cardiovascular protective effects in patients with CKD; however, their long-term effects in patients with AS and the underlying mechanisms remain to be clarified.
methodsWe conducted a single-arm, prospective study to examine the effect of dapagliflozin in patients with AS. In parallel, Col4a3 p.C1615Y-mutant mice (129S2/Sv background) were used as an AS model to investigate the renoprotective mechanisms of dapagliflozin.
resultsA total of twenty-one patients with AS were enrolled. After approximately 12 months of follow-up (12.6±1.2 months), the mean 24-hour urinary protein decreased by 29% to 1.25±0.73 g from baseline (1.75±0.90; P < 0.001). The eGFR showed no significant difference compared with baseline (76±28 versus 77±29 ml/min per 1.73 m 2 , P = 0.57). In the animal studies, dapagliflozin significantly reduced macrophage infiltration and the expression of inflammatory cytokines levels in the renal cortex of Col4a3 -mutant mice. Mechanistic studies showed that stimulator of IFN genes (STING) pathway was activated in the renal cortex and tubular epithelial cells (TECs) from Col4a3 mice, contributing to a proinflammatory phenotype. Dapagliflozin effectively inhibited STING activation and suppressed inflammatory cytokines production in mutant TECs.
conclusionsDapagliflozin can reduce proteinuria in patients with AS and plays an anti-inflammatory role by inhibiting the STING pathway in TECs of AS mice.
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