ArticleThe Journal of urology2015
Transcriptional dysregulation in the ureteric bud causes multicystic dysplastic kidney by branching morphogenesis defect.
Article in The Journal of urology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Influence of Obstructive Uropathy on Cyst Formation and Nephrogenesis: Insights from a Fetal Lamb Model.Journal of developmental biology · 2026Article
- Pathophysiology of Congenital Anomalies of the Kidney and Urinary Tract: A Comprehensive Review.Cells · 2024Review
- Early diagnosis of solitary functioning kidney: comparing the prognosis of kidney agenesis and multicystic dysplastic kidney.Pediatric nephrology (Berlin, Germany) · 2024Article
- Minimally invasive open nephrectomy on children with multicystic dysplastic kidney.Experimental and therapeutic medicine · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe calcineurin-NFAT signaling pathway regulates the transcription of genes important for development. It is impacted by various genetic and environmental factors. We investigated the potential role of NFAT induced transcriptional dysregulation in the pathogenesis of congenital abnormalities of the kidneys and urinary tract. MATERIALS AND
methodsA murine model of conditional NFATc1 activation in the ureteric bud was generated and examined for histopathological changes. Metanephroi were also cultured in vitro to analyze branching morphogenesis in real time.
resultsNFATc1 activation led to defects resembling multicystic dysplastic kidney. These mutants showed severe disorganization of branching morphogenesis characterized by decreased ureteric bud branching and the disconnection of ureteric bud derivatives from the main collecting system. The orphan ureteric bud derivatives may have continued to induce nephrogenesis and likely contributed to the subsequent formation of blunt ended filtration units and cysts. The ureter also showed irregularities consistent with impaired epithelial-mesenchymal interaction.
conclusionsThis study reveals the profound effects of NFAT signaling dysregulation on the ureteric bud and provides insight into the pathogenesis of multicystic dysplastic kidney. Our results suggest that the obstruction hypothesis and the bud theory may not be mutually exclusive to explain the pathogenesis of multicystic dysplastic kidney. Ureteric bud dysfunction such as that induced by NFAT activation can disrupt ureteric bud-metanephric mesenchyma interaction, causing primary defects in branching morphogenesis, subsequent dysplasia and cyst formation. Obstruction of the main collecting system can further enhance these defects, producing the pathological changes associated with multicystic dysplastic kidney.
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