ArticleJournal of the American Society of Nephrology : JASN2015
Activation of Notch3 in Glomeruli Promotes the Development of Rapidly Progressive Renal Disease.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- Broadening horizons: Pathogenesis and therapeutics of renal ciliopathies.Journal of cell communication and signaling · 2026Review
- A Clinical Genetics-Driven Dual Diagnosis of Prader-Willi Syndrome Due to Mosaic Maternal UPD(15) andGenes · 2026Article
- Endothelial cells regulate mesangial cells through the Dll4/Notch3 axis to participate in glomerular injury in lupus nephritis.Frontiers in immunology · 2026Article
- Extracellular Vesicular Proteins in Plasma from Patients with Cutaneous Lupus Correlate with Disease Activity.Current issues in molecular biology · 2025Article
- Article
- Kidney transcriptomics signature of prospective rapid diabetic kidney disease progression.BMC nephrology · 2025Article
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.Disease models & mechanisms · 2025Article
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.bioRxiv : the preprint server for biology · 2024Article
- A preliminary study of the miRNA restitution effect on CNV-induced miRNA downregulation in CAKUT.BMC genomics · 2024Article
- N6-methyladenosine methylation in kidney injury.Clinical epigenetics · 2023Review
- Polycystic kidneys: interaction of notch and renin.Clinical science (London, England : 1979) · 2023Article
- Notch Signaling in Acute Inflammation and Sepsis.International journal of molecular sciences · 2023Review
- Calreticulin in renal fibrosis: A short review.Journal of cellular and molecular medicine · 2022Review
- Notch3 expression in capillary pericytes predicts worse graft outcome in human renal grafts with antibody-mediated rejection.Journal of cellular and molecular medicine · 2022Article
- Epigenetic Modulation of Gremlin-1/NOTCH Pathway in Experimental Crescentic Immune-Mediated Glomerulonephritis.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Activation of Notch3 in Renal Tubular Cells Leads to Progressive Cystic Kidney Disease.International journal of molecular sciences · 2022Article
- MAD2B promotes podocyte injury through regulating Numb-dependent Notch 1 pathway in diabetic nephropathy.International journal of biological sciences · 2022Article
- Glucocorticoids Inhibit EGFR Signaling Activation in Podocytes in Anti-GBM Crescentic Glomerulonephritis.Frontiers in medicine · 2022Article
- Roles of SIRT6 in kidney disease: a novel therapeutic target.Cellular and molecular life sciences : CMLS · 2021Article
- Transcriptomic data showing differentially expressed genes between Notch3 and Notch4 deleted mice.Data in brief · 2021Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Notch3 expression is found in the glomerular podocytes of patients with lupus nephritis or focal segmental GN but not in normal kidneys. Here, we show that activation of the Notch3 receptor in the glomeruli is a turning point inducing phenotypic changes in podocytes promoting renal inflammation and fibrosis and leading to disease progression. In a model of rapidly progressive GN, Notch3 expression was induced by several-fold in podocytes concurrently with disease progression. By contrast, mice lacking Notch3 expression were protected because they exhibited less proteinuria, uremia, and inflammatory infiltration. Podocyte outgrowth from glomeruli isolated from wild-type mice during the early phase of the disease was higher than outgrowth from glomeruli of mice lacking Notch3. In vitro studies confirmed that podocytes expressing active Notch3 reorganize their cytoskeleton toward a proliferative/migratory and inflammatory phenotype. We then administered antisense oligodeoxynucleotides targeting Notch3 or scramble control oligodeoxynucleotides in wild-type mice concomitant to disease induction. Both groups developed chronic renal disease, but mice injected with Notch3 antisense had lower values of plasma urea and proteinuria and inflammatory infiltration. The improvement of renal function was accompanied by fewer deposits of fibrin within the glomeruli and by decreased peritubular inflammation. Finally, abnormal Notch3 staining was observed in biopsy samples of patients with crescentic GN. These results demonstrate that abnormal activation of Notch3 may be involved in the progression of renal disease by promoting migratory and proinflammatory pathways. Inhibiting Notch3 activation could be a novel, promising approach to treat GN.
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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.