ReviewKidney international2015
Towards an understanding of kidney diseases associated with WT1 mutations.
Review in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05875454 (Assessment of Podocyts Integrity in Glomerular Diseases.), which is not on this map. Cited by 45 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Assessment of Podocyts Integrity in Glomerular Diseases.
Who cites it
45 citing papers in PubMed, 73 citations in OpenAlex.
- Upregulation of PTPRO by WT1 alleviates podocyte injury in diabetic nephropathy through inhibiting the c-Abl/p53 pathway.Cellular and molecular life sciences : CMLS · 2026Article
- Article
- Serial Kidney Biopsies Reveal Progressive Pathology in Townes-Brocks Syndrome: A Case Report.Kidney medicine · 2026Article
- PHENOCAUZ: Linking Human Symptoms, Drug Side Effects and Efficacy to Their Molecular Causes Using Mendelian Disease Biology.bioRxiv : the preprint server for biology · 2026Article
- Advances in SRNS Gene Research: From Precision Classification to Precision Diagnosis and Treatment.Biomedicines · 2026Review
- Tumor-Associated Macrophage Polarization in Wilms' Tumor After Neoadjuvant Chemotherapy.Cancers · 2026Article
- SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Podocytopathies.Nature reviews. Disease primers · 2025Review
- Single-cell sequencing and organoids: applications in organ development and disease.Molecular biomedicine · 2025Review
- WT1 gene: a potential therapeutic target for multiple cancer treatment strategies.Clinical and experimental medicine · 2025Review
- Mechanisms of podocyte injury in genetic kidney disease.Pediatric nephrology (Berlin, Germany) · 2025Review
- Article
- The mechanism of enterogenous toxin methylmalonic acid aggravating calcium-phosphorus metabolic disorder in uremic rats by regulating the Wnt/β-catenin pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- A review of the genetic background in complicated WT1-related disorders.Clinical and experimental nephrology · 2025Review
- Concomitant Wilms tumor and autosomal dominant polycystic kidney disease.Pediatric blood & cancer · 2024Article
- Article
- Inter-Ethnic Variations in the Clinical, Pathological, and Molecular Characteristics of Wilms Tumor.Cancers · 2024Review
- Kidney Organoid Modeling of WT1 Mutations Reveals Key Regulatory Paths Underlying Podocyte Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Upregulation of HOXA3 by isoform-specific Wilms tumour 1 drives chemotherapy resistance in acute myeloid leukaemia.British journal of haematology · 2024Article
- Multiplexed bulk and single-cell RNA-seq hybrid enables cost-efficient disease modeling with chimeric organoids.Nature communications · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in Wilms' tumor 1 (WT1) cause a wide spectrum of renal manifestations, eventually leading to end-stage kidney failure. Insufficient understanding of WT1's molecular functions in kidney development has hampered efficient therapeutic applications for WT1-associated diseases. Recently, the generation and characterization of mouse models and application of multiple state-of-the-art approaches have significantly expanded our understanding of the molecular mechanisms of how WT1 mutations lead to kidney failure. Here, we discuss the WT1 binding consensus and illustrate the major roles of WT1 in different cell populations in kidney biology. WT1 controls metanephric mesenchyme (MM) self-renewal and proliferation mainly by regulating FGF and BMP-pSMAD signaling pathways as well as Sall1 and Pax2, encoding key transcription factors; WT1 drives MM differentiation and mesenchyme-epithelial transition by targeting Fgf8 and Wnt4; WT1 defines podocyte identity by activation of other podocyte-specific transcription factors, including Mafb, Lmx1b, FoxC2, and Tcf21. These factors potentially cooperate with WT1 regulating the expression of components and regulators of the cytoskeleton for establishing podocyte polarity, slit diaphragm structure, and focal adhesion to the glomerular basement membrane. Understanding of WT1's function in kidney biology including WT1-regulated pathways will give insights that will eventually help therapeutic applications.
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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.