ArticleClinical science (London, England : 1979)2023
Overexpression of notch signaling in renin cells leads to a polycystic kidney phenotype.
Article in Clinical science (London, England : 1979), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Preterm Birth Increases Susceptibility to Hyperglycemia-Induced Kidney Injury With Sex-Specific Differences in Structural and Molecular Responses.Endocrinology, diabetes & metabolism · 2026Article
- Abnormal purinergic signaling contributes to development of renal cysts in autosomal dominant polycystic kidney disease.Purinergic signalling · 2026Article
- Preterm birth increases susceptibility to hyperglycemia induced glomerular alterations in male mice.Scientific reports · 2025Article
- Notch2 Inhibition and Kidney Cyst Growth in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025Article
- Electrolyte and metabolite composition of cystic fluid from a rat model of ARPKD.Communications biology · 2025Article
- Notch signaling in diabetic kidney disease: recent progress.Frontiers in endocrinology · 2025Review
- Polycystic kidneys: interaction of notch and renin.Clinical science (London, England : 1979) · 2023Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Polycystic kidney disease (PKD) is an inherited disorder that results in large kidneys, numerous fluid-filled cysts, and ultimately end-stage kidney disease. PKD is either autosomal dominant caused by mutations in PKD1 or PKD2 genes or autosomal recessive caused by mutations in the PKHD1 or DZIP1L genes. While the genetic basis of PKD is known, the downstream molecular mechanisms and signaling pathways that lead to deregulation of proliferation, apoptosis, and differentiation are not completely understood. The Notch pathway plays critical roles during kidney development including directing differentiation of various progenitor cells, and aberrant Notch signaling results in gross alternations in cell fate. In the present study, we generated and studied transgenic mice that have overexpression of an intracellular fragment of mouse Notch1 ('NotchIC') in renin-expressing cells. Mice with overexpression of NotchIC in renin-expressing cells developed numerous fluid-filled cysts, enlarged kidneys, anemia, renal insufficiency, and early death. Cysts developed in both glomeruli and proximal tubules, had increased proliferation marks, and had increased levels of Myc. The present work implicates the Notch signaling pathway as a central player in PKD pathogenesis and suggests that the Notch-Myc axis may be an important target for therapeutic intervention.
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