ArticleJournal of the American Society of Nephrology : JASN2015
Nephrin Preserves Podocyte Viability and Glomerular Structure and Function in Adult Kidneys.
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 70 papers.
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Who cites it
70 citing papers in PubMed, 127 citations in OpenAlex.
- SGLT2 inhibitors attenuate nephrin loss and enhance TGF-βScientific reports · 2022Trial
- Wnt/β-Catenin Signaling in Diabetic Complications: Mechanisms and Therapeutic Potential.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Benzo[b]fluoranthene is involved in idiopathic membranous nephropathy by inducing podocyte injury.Journal of translational internal medicine · 2025Article
- SA4503 Mitigates Adriamycin-Induced Nephropathy via Sigma-1 Receptor in Animal and Cell-Based Models.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Cyclin-dependent kinase 5 as a potential therapeutic target to alleviate high glucose-induced podocyte apoptosis and hyperglycemia-induced renal injury in mice.Histology and histopathology · 2025Article
- Mechanosensitive Differentiation of Human iPS Cell-Derived Podocytes.Bioengineering (Basel, Switzerland) · 2024Article
- Urolithin A Ameliorates the TGF Beta-Dependent Impairment of Podocytes Exposed to High Glucose.Journal of personalized medicine · 2024Article
- Article
- C5a-C5aR1 axis controls mitochondrial fission to promote podocyte injury in lupus nephritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Central role of podocytes in mediating cellular cross talk in glomerular health and disease.American journal of physiology. Renal physiology · 2024Review
- Reciprocal regulation of SIRT1 and AMPK by Ginsenoside compound K impedes the conversion from plasma cells to mitigate for podocyte injury in MRL/Journal of ginseng research · 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
- Piperazine ferulate inhibits diabetic nephropathy by suppressing AGE/RAGE-mediated inflammatory signaling in rats and podocytes.Frontiers in pharmacology · 2024Article
- To Explore the Putative Molecular Targets of Diabetic Nephropathy and their Inhibition Utilizing Potential Phytocompounds.Current medicinal chemistry · 2024Review
- High mobility group box 1 (HMGB1) mediates nicotine-induced podocyte injury.Frontiers in pharmacology · 2024Article
- URINARY NEPHRIN AS AN EARLY BIOMARKER OF HYPERTENSIVE NEPHROPATHY.Acta clinica Croatica · 2023Article
- Sex differences in long-term kidney fibrosis following neonatal nephron loss during ongoing nephrogenesis.Molecular and cellular pediatrics · 2023Article
- Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy.Frontiers in immunology · 2023Review
- Research progress of natural active compounds on improving podocyte function to reduce proteinuria in diabetic kidney disease.Renal failure · 2023Review
- Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 8 institutions in 2 countries.
Funding
Abstract
Nephrin is required during kidney development for the maturation of podocytes and formation of the slit diaphragm junctional complex. Because nephrin expression is downregulated in acquired glomerular diseases, nephrin deficiency is considered a pathologic feature of glomerular injury. However, whether nephrin deficiency exacerbates glomerular injury in glomerular diseases has not been experimentally confirmed. Here, we generated mice with inducible RNA interference-mediated nephrin knockdown. Short-term nephrin knockdown (6 weeks), starting after the completion of kidney development at 5 weeks of age, did not affect glomerular structure or function. In contrast, mice with long-term nephrin knockdown (20 weeks) developed mild proteinuria, foot process effacement, filtration slit narrowing, mesangial hypercellularity and sclerosis, glomerular basement membrane thickening, subendothelial zone widening, and podocyte apoptosis. When subjected to an acquired glomerular insult induced by unilateral nephrectomy or doxorubicin, mice with short-term nephrin knockdown developed more severe glomerular injury compared with mice without nephrin knockdown. Additionally, nephrin-knockdown mice developed more exaggerated glomerular enlargement when subjected to unilateral nephrectomy and more podocyte apoptosis and depletion after doxorubicin challenge. AKT phosphorylation, which is a slit diaphragm-mediated and nephrin-dependent pathway in the podocyte, was markedly reduced in mice with long-term or short-term nephrin knockdown challenged with uninephrectomy or doxorubicin. Taken together, our data establish that under the basal condition and in acquired glomerular diseases, nephrin is required to maintain slit diaphragm integrity and slit diaphragm-mediated signaling to preserve glomerular function and podocyte viability in adult mice.
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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.