ArticleCell reports. Medicine2024
The SGLT2 inhibitor dapagliflozin ameliorates renal fibrosis in hyperuricemic nephropathy.
Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- SGLT2 inhibitors: mechanisms, physiology and pharmacology, and clinical applications.Molecular biomedicine · 2026Review
- SGLT2 Inhibitors in Nephrolithiasis: Emerging Evidence and What Urologists Need to Know.Medical sciences (Basel, Switzerland) · 2026Review
- Multi-omics-driven precision medicine.iMeta · 2026Review
- Blue Honeysuckle Extract Ameliorates Hyperuricemia by Modulating Gut Microbiota and Improving Liver-Kidney-Gut Axis Function.Antioxidants (Basel, Switzerland) · 2026Article
- Hirudin Attenuates Uric Acid-Induced Renal Tubular Injury via TNFRSF6B-Mediated Suppression of NF-κB Signaling.Pharmacology research & perspectives · 2026Article
- NSUN5 Attenuates Renal Injury and Ferroptosis in Hyperuricaemic Nephropathy Through YBX2-Dependent Stabilisation of SCD1 m5C Methylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- GAS5 mediates notch signaling to exacerbate calcium oxalate-induced renal injury through the NF-κB/NLRP3 axis by promoting macrophage polarization.Cellular and molecular life sciences : CMLS · 2026Article
- The core mechanism of hypertension-linked renal fibrosis: "RAAS-ROS-inflammation-fibrosis" axis.iScience · 2026Review
- GPR109a-AMPK axis mediates the Attenuation of uric acid-induced M1 macrophage polarization by β-hydroxybutyrate from Lacticaseibacillus rhamnosus M2b.Scientific reports · 2026Article
- Targeting MYC in T-Cell lymphoma via epigenetic modulation with a small-molecule inhibitor.Molecular cancer · 2026Article
- ERRα-NOS2-mediated citrulline metabolism attenuates tubular epithelial cell senescence in diabetic kidney disease.Redox biology · 2026Article
- Emerging therapeutic pipelines on kidney fibrosis: challenges in translational research.Journal of translational medicine · 2026Review
- Chronic Kidney Disease in Metabolic Disease: Regulation of SGLT2 and Transcriptomic-Epigenetic Effects of Its Pharmacological Inhibition.International journal of molecular sciences · 2026Review
- Current understanding of sodium-glucose transporter 2 inhibitors in cardiovascular-kidney-metabolic syndrome.Frontiers in pharmacology · 2026Review
- Proteins and signalling pathways targeted by dapagliflozin and finerenone: Insights from DAPA-CKD and FIGARO-DKD.Diabetes, obesity & metabolism · 2026Article
- Antiproteinuric effect of dapagliflozin attenuates tubule-interstitial injury development in subclinical acute kidney injury animal model.Frontiers in pharmacology · 2026Article
- The double-edged sword effect of estrogen in kidney disease and its precision modulation.Frontiers in endocrinology · 2026Review
- Association Between Triglyceride-Glucose Index and Hyperuricemia in Hospitalized Patients with Depression: A Cross-Sectional Study.Neuropsychiatric disease and treatment · 2026Article
- Review
- State of the art: Renal recovery after AKI - from basic science to clinical practice.Intensive care medicine · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
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Abstract
Hyperuricemic nephropathy (HN) is a global metabolic disorder characterized by uric acid (UA) metabolism dysfunction, resulting in hyperuricemia (HUA) and tubulointerstitial fibrosis (TIF). Sodium-dependent glucose transporter 2 inhibitor, dapagliflozin, has shown potential in reducing serum UA levels in patients with chronic kidney disease (CKD), though its protective effects against HN remain uncertain. This study investigates the functional, pathological, and molecular changes in HN through histological, biochemical, and transcriptomic analyses in patients, HN mice, and UA-stimulated HK-2 cells. Findings indicate UA-induced tubular dysfunction and fibrotic activation, which dapagliflozin significantly mitigates. Transcriptomic analysis identifies estrogen-related receptor α (ERRα), a downregulated transcription factor in HN. ERRα knockin mice and ERRα-overexpressed HK-2 cells demonstrate UA resistance, while ERRα inhibition exacerbates UA effects. Dapagliflozin targets ERRα, activating the ERRα-organic anion transporter 1 (OAT1) axis to enhance UA excretion and reduce TIF. Furthermore, dapagliflozin ameliorates renal fibrosis in non-HN CKD models, underscoring the therapeutic significance of the ERRα-OAT1 axis in HN and CKD.
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