ArticleJournal of the American Society of Nephrology : JASN2008
Ectopic notch activation in developing podocytes causes glomerulosclerosis.
Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.
- The Impact of Omega Fatty Acids on DKD: A Multimodal Study Integrating Mendelian Randomization, Proteomic Mediation Analysis, and Meta-Analysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Pooled it
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.Disease models & mechanisms · 2025Article
- Podocyte, tubular epithelial-immune cell interplay in the pathogenesis of lupus nephritis.Frontiers in immunology · 2025Review
- The Pathogenesis of Nephrotic Syndrome: A Perspective from B Cells.Kidney diseases (Basel, Switzerland) · 2024Review
- Podocyte-targeted therapies - progress and future directions.Nature reviews. Nephrology · 2024Review
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.bioRxiv : the preprint server for biology · 2024Article
- Blockade of Notch1 Signaling Alleviated Podocyte Injury in Lupus Nephritis Via Inhibition of NLRP3 Inflammasome Activation.Inflammation · 2024Article
- Senolytic combination of dasatinib and quercetin protects against diabetic kidney disease by activating autophagy to alleviate podocyte dedifferentiation via the Notch pathway.International journal of molecular medicine · 2024Article
- Cytoplasmic WT1 in IgA nephropathy, an indicator of poor prognosis associated with mesangial/peri-mesangial C4d.International urology and nephrology · 2023Article
- Differences in Immunohistochemical and Ultrastructural Features between Podocytes and Parietal Epithelial Cells (PECs) Are Observed in Developing, Healthy Postnatal, and Pathologically Changed Human Kidneys.International journal of molecular sciences · 2022Article
- Revisiting the role of Notch in nephron segmentation confirms a role for proximal fate selection during mouse and human nephrogenesis.Development (Cambridge, England) · 2022Article
- Epigenetic Modulation of Gremlin-1/NOTCH Pathway in Experimental Crescentic Immune-Mediated Glomerulonephritis.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Integrated analysis of potential gene crosstalk between non-alcoholic fatty liver disease and diabetic nephropathy.Frontiers in endocrinology · 2022Article
- Targeted disruption of the histone lysine 79 methyltransferase Dot1L in nephron progenitors causes congenital renal dysplasia.Epigenetics · 2021Article
- Activation of Notch1 signaling in podocytes by glucose-derived AGEs contributes to proteinuria.BMJ open diabetes research & care · 2020Article
- Mutations in LAMB2 Are Associated With Albuminuria and Optic Nerve Hypoplasia With Hypopituitarism.The Journal of clinical endocrinology and metabolism · 2020Article
- The Role of Notch3 Signaling in Kidney Disease.Oxidative medicine and cellular longevity · 2020Review
- Notch4 activation aggravates NF-κB-mediated inflammation in HIV-1-associated nephropathy.Disease models & mechanisms · 2019Article
- Notch Signaling in Kidney Development, Maintenance, and Disease.Biomolecules · 2019Review
15 more citing papers are in PubMed but not listed here.
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8 authors at 2 institutions in 1 country.
Funding
Abstract
Genetic evidence supports an early role for Notch signaling in the fate of podocytes during glomerular development. Decreased expression of Notch transcriptional targets in developing podocytes after the determination of cell fate suggests that constitutive Notch signaling may oppose podocyte differentiation. This study determined the effects of constitutive Notch signaling on podocyte differentiation by ectopically expressing Notch's intracellular domain (NOTCH-IC), the biologically active, intracellular product of proteolytic cleavage of the Notch receptor, in developing podocytes of transgenic mice. Histologic and molecular analyses revealed normal glomerular morphology and expression of podocyte markers in newborn NOTCH-IC-expressing mice; however, mice developed severe proteinuria and showed evidence of progressive glomerulosclerosis at 2 wk after birth. Features of mature podocytes were lost: Foot processes were effaced; expression of Wt1, Nphs1, and Nphs2 was downregulated; cell-cycle re-entry was induced; and the expression of Pax2 was increased. In contrast, mice with podocyte-specific inactivation of Rbpsuh, which encodes a protein essential for canonical Notch signaling, seemed normal. In addition, the damaging effects of NOTCH-IC expression were prevented in transgenic mice after simultaneous conditional inactivation of Rbpsuh in murine podocytes. These results suggest that Notch signaling is dispensable during terminal differentiation of podocytes but that constitutive (or inappropriate) Notch signaling is deleterious, leading to glomerulosclerosis.
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Registered trials
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