ArticleJournal of the American Society of Nephrology : JASN2011
TGF-alpha mediates genetic susceptibility to chronic kidney disease.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
- Dynamic single-nucleus transcriptomic profiling of kidney development in Bamaxiang pigs and wild boar.Zoological research · 2026Article
- Recessive variants in the intergenic NOS1AP-C1orf226 locus cause monogenic kidney disease responsive to anti-proteinuric treatment.Nature communications · 2025Article
- Chronic kidney disease.Nature reviews. Disease primers · 2025Review
- Plasma MCP-1 and TGF-β1 Levels are Associated with Kidney Injury in Children with Congenital Anomalies of the Kidney and Urinary Tract.Applied biochemistry and biotechnology · 2024Article
- Development and Characterization of a Novel FVB-Genes · 2024Article
- Signaling pathways predisposing to chronic kidney disease progression.JCI insight · 2020Article
- The Blockade of TACE-Dependent EGF Receptor Activation by Losartan-Erlotinib Combination Attenuates Renal Fibrosis Formation in 5/6-Nephrectomized Rats Under Vitamin D Deficiency.Frontiers in medicine · 2020Article
- Article
- Krüppel-like factor 4 is a negative regulator of STAT3-induced glomerular epithelial cell proliferation.JCI insight · 2018Article
- Role of Epidermal Growth Factor Receptor (EGFR) and Its Ligands in Kidney Inflammation and Damage.Mediators of inflammation · 2018Review
- Spindle pole cohesion requires glycosylation-mediated localization of NuMA.Scientific reports · 2017Article
- Stat3 Controls Tubulointerstitial Communication during CKD.Journal of the American Society of Nephrology : JASN · 2016Article
- Increased urinary lysophosphatidic acid in mouse with subtotal nephrectomy: potential involvement in chronic kidney disease.Journal of physiology and biochemistry · 2016Article
- Structural basis of selectivity and neutralizing activity of a TGFα/epiregulin specific antibody.Protein science : a publication of the Protein Society · 2016Article
- Role of Receptor Tyrosine Kinase Signaling in Renal Fibrosis.International journal of molecular sciences · 2016Review
- Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice.PloS one · 2016Article
- Genetic Background is a Key Determinant of Glomerular Extracellular Matrix Composition and Organization.Journal of the American Society of Nephrology : JASN · 2015Article
- Activation of Notch3 in Glomeruli Promotes the Development of Rapidly Progressive Renal Disease.Journal of the American Society of Nephrology : JASN · 2015Article
- Phosphorylation of ribosomal protein S6 mediates compensatory renal hypertrophy.Kidney international · 2015Article
- Causes and pathogenesis of focal segmental glomerulosclerosis.Nature reviews. Nephrology · 2015Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms of progression of chronic kidney disease (CKD) are poorly understood. Epidemiologic studies suggest a strong genetic component, but the genes that contribute to the onset and progression of CKD are largely unknown. Here, we applied an experimental model of CKD (75% excision of total renal mass) to six different strains of mice and found that only the FVB/N strain developed renal lesions. We performed a genome-scan analysis in mice generated by back-crossing resistant and sensitive strains; we identified a major susceptibility locus (Ckdp1) on chromosome 6, which corresponds to regions on human chromosome 2 and 3 that link with CKD progression. In silico analysis revealed that the locus includes the gene encoding the EGF receptor (EGFR) ligand TGF-α. TGF-α protein levels markedly increased after nephron reduction exclusively in FVB/N mice, and this increase preceded the development of renal lesions. Furthermore, pharmacologic inhibition of EGFR prevented the development of renal lesions in the sensitive FVB/N strain. These data suggest that variable TGF-α expression may explain, in part, the genetic susceptibility to CKD progression. EGFR inhibition may be a therapeutic strategy to counteract the genetic predisposition to CKD.
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Registered trials
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.