ArticleJournal of the American Society of Nephrology : JASN2015
EGF Receptor Inhibition Alleviates Hyperuricemic Nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 121 citations in OpenAlex.
- Polydatin alleviates adenine-induced nephropathy in mice.Renal failure · 2026Article
- Ubiquitin-specific protease 11 facilitates the activation and proliferation of renal interstitial fibroblasts through epidermal growth factor receptor signaling pathways.Renal failure · 2026Article
- Targeting Cathepsin B with p-coumaric acid rescues WWP1-dependent proteasomal degradation of NLRP3 in hyperuricemic nephropathy.Molecular medicine (Cambridge, Mass.) · 2026Article
- The Positive Feedback Loop of Hypoxia-Inducible Factor-1 α /miR-295/Factor Inhibiting Hypoxia-Inducible Factor-1 in Hyperuricemic Nephropathy.Kidney360 · 2026Article
- Inhibition of purine nucleoside and nucleobase transporters by tyrosine kinase inhibitors.PloS one · 2026Article
- Environmental cadmium exposure aggravates renal fibrosis and reduced renal lipid accumulation in diabetic mice.Lipids in health and disease · 2025Article
- The Long-Term Effects of the Selective Inhibitor of Urate Transporter 1, Dotinurad, on Metabolic Parameters and Renal Function in Japanese Patients With Asymptomatic Hyperuricemia.Journal of clinical medicine research · 2025Article
- Compound probiotics alleviate hyperuricemia-induced renal injury via restoring gut microbiota and metabolism.BMC microbiology · 2025Article
- Insights into renal damage in hyperuricemia: Focus on renal protection (Review).Molecular medicine reports · 2025Review
- Spatiotemporal landscape of kidney in a mouse model of hyperuricemia at single-cell level.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy.Current molecular medicine · 2025Article
- Tigulixostat Alleviates Hyperuricemic Nephropathy by Promoting M2 Macrophage Polarization.Journal of inflammation research · 2025Article
- Recent Advances on the Regulations of Organic Anion Transporters.Pharmaceutics · 2024Review
- Direct GPCR-EGFR interaction enables synergistic membrane-to-nucleus information transfer.Cellular and molecular life sciences : CMLS · 2024Article
- Mechanisms of norcantharidin against renal tubulointerstitial fibrosis.Pharmacological reports : PR · 2024Review
- Caspase-11/GSDMD contributes to the progression of hyperuricemic nephropathy by promoting NETs formation.Cellular and molecular life sciences : CMLS · 2024Article
- Anti-Hyperuricemic Effects of Extracts fromMetabolites · 2024Article
- Pharmacological inhibition of Src family kinases attenuates hyperuricemic nephropathy.Frontiers in pharmacology · 2024Article
- Fisetin ameliorates fibrotic kidney disease in mice via inhibiting ACSL4-mediated tubular ferroptosis.Acta pharmacologica Sinica · 2024Article
- The effect of lipid metabolism disorder on patients with hyperuricemia using Multi-Omics analysis.Scientific reports · 2023Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Hyperuricemia is an independent risk factor for CKD and contributes to kidney fibrosis. In this study, we investigated the effect of EGF receptor (EGFR) inhibition on the development of hyperuricemic nephropathy (HN) and the mechanisms involved. In a rat model of HN induced by feeding a mixture of adenine and potassium oxonate, increased EGFR phosphorylation and severe glomerular sclerosis and renal interstitial fibrosis were evident, accompanied by renal dysfunction and increased urine microalbumin excretion. Administration of gefitinib, a highly selective EGFR inhibitor, prevented renal dysfunction, reduced urine microalbumin, and inhibited activation of renal interstitial fibroblasts and expression of extracellular proteins. Gefitinib treatment also inhibited hyperuricemia-induced activation of the TGF-β1 and NF-κB signaling pathways and expression of multiple profibrogenic cytokines/chemokines in the kidney. Furthermore, gefitinib treatment suppressed xanthine oxidase activity, which mediates uric acid production, and preserved expression of organic anion transporters 1 and 3, which promotes uric acid excretion in the kidney of hyperuricemic rats. Thus, blocking EGFR can attenuate development of HN via suppression of TGF-β1 signaling and inflammation and promotion of the molecular processes that reduce uric acid accumulation in the body.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.