ArticleKidney international2018
Activation of podocyte Notch mediates early Wt1 glomerulopathy.
Article in Kidney international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- MiR-423-5p inhibition alleviates podocyte apoptosis in membranous nephropathy by targeting WT1/β-catenin axis.International urology and nephrology · 2026Article
- Single-cell and high-resolution spatial profiling of podocytopathies reveals core mechanisms of podocyte injury.Science advances · 2026Article
- Article
- Notch2 Inhibition and Kidney Cyst Growth in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025Article
- Role of mZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Growth and differentiation of human induced pluripotent stem cell (hiPSC)-derived kidney organoids using fully synthetic peptide hydrogels.Bioactive materials · 2023Article
- WT1Theranostics · 2023Article
- Network-based identification and prioritization of key transcriptional factors of diabetic kidney disease.Computational and structural biotechnology journal · 2023Article
- Podocytes are lost from glomeruli before completing apoptosis.American journal of physiology. Renal physiology · 2022Article
- WT1 complete gonadal dysgenesis with membranoproliferative glomerulonephritis: case series and literature review.Pediatric nephrology (Berlin, Germany) · 2022Review
- Epigenetic Modulation of Gremlin-1/NOTCH Pathway in Experimental Crescentic Immune-Mediated Glomerulonephritis.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Cellular phenotypic transitions in diabetic nephropathy: An update.Frontiers in pharmacology · 2022Review
- The recruitment mechanisms and potential therapeutic targets of podocytes from parietal epithelial cells.Journal of translational medicine · 2021Review
- PP2A protects podocytes against Adriamycin-induced injury and epithelial-to-mesenchymal transition via suppressing JIP4/p38-MAPK pathway.Cytotechnology · 2021Article
- Super-Enhancer-Associated Transcription Factors Maintain Transcriptional Regulation in Mature Podocytes.Journal of the American Society of Nephrology : JASN · 2021Article
- A novel WT1 gene mutation in a chinese girl with denys-drash syndrome.Journal of clinical laboratory analysis · 2021Article
- Mutations inJournal of the American Society of Nephrology : JASN · 2021Article
- Bioinformatics analysis of genes related to iron death in diabetic nephropathy through network and pathway levels based approaches.PloS one · 2021Article
- PPARγ Mediates the Anti-Epithelial-Mesenchymal Transition Effects of FGF1Frontiers in pharmacology · 2021Article
- A Partial Picture of the Single-Cell Transcriptomics of Human IgA Nephropathy.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
The Wilms' tumor suppressor gene, WT1, encodes a zinc finger protein that regulates podocyte development and is highly expressed in mature podocytes. Mutations in the WT1 gene are associated with the development of renal failure due to the formation of scar tissue within glomeruli, the mechanisms of which are poorly understood. Here, we used a tamoxifen-based CRE-LoxP system to induce deletion of Wt1 in adult mice to investigate the mechanisms underlying evolution of glomerulosclerosis. Podocyte apoptosis was evident as early as the fourth day post-induction and increased during disease progression, supporting a role for Wt1 in mature podocyte survival. Podocyte Notch activation was evident at disease onset with upregulation of Notch1 and its transcriptional targets, including Nrarp. There was repression of podocyte FoxC2 and upregulation of Hey2 supporting a role for a Wt1/FoxC2/Notch transcriptional network in mature podocyte injury. The expression of cleaved Notch1 and HES1 proteins in podocytes of mutant mice was confirmed in early disease. Furthermore, induction of podocyte HES1 expression was associated with upregulation of genes implicated in epithelial mesenchymal transition, thereby suggesting that HES1 mediates podocyte EMT. Lastly, early pharmacological inhibition of Notch signaling ameliorated glomerular scarring and albuminuria. Thus, loss of Wt1 in mature podocytes modulates podocyte Notch activation, which could mediate early events in WT1-related glomerulosclerosis.
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Registered trials
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