ArticleJournal of the American Society of Nephrology : JASN2009
Podocin inactivation in mature kidneys causes focal segmental glomerulosclerosis and nephrotic syndrome.
Article in Journal of the American Society of Nephrology : JASN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 108 citations in OpenAlex.
- Disease-driven post-transcriptional alterations and alternative splicing in podocytes in focal segmental glomerulosclerosis.EMBO molecular medicine · 2026Article
- Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndrome.Pflugers Archiv : European journal of physiology · 2026Article
- Podocyte injury damages podocytes in chimeric organoids.PloS one · 2026Article
- Podocytopathies.Nature reviews. Disease primers · 2025Review
- Lysosome stress response and mitochondria injury are the earliest detectable alteration in FSGS.Scientific reports · 2025Article
- A red fluorescent lifeact marker to study actin morphology in podocytes.Scientific reports · 2025Article
- Glucosylceramide synthase modulation ameliorates murine renal pathologies and promotes macrophage effector function in vitro.Communications biology · 2024Article
- PIK3CA inhibition in models of proliferative glomerulonephritis and lupus nephritis.The Journal of clinical investigation · 2024Article
- Filtration and tubular handling of EWE-hC3Nb1, a complement inhibitor nanobody, in wild type mice and a mouse model of proteinuric kidney disease.FEBS open bio · 2024Article
- Adriamycin-induced podocyte injury via the Sema3A/TRPC5/Rac1 pathway.Frontiers in medicine · 2024Article
- The influence of calcitriol and methylprednisolone on podocytes function in minimal change disease in vitro model.Scientific reports · 2023Article
- Ang-(1-7) attenuates podocyte injury induced by high glucoseArchives of endocrinology and metabolism · 2023Article
- Current understanding of the molecular mechanisms of circulating permeability factor in focal segmental glomerulosclerosis.Frontiers in immunology · 2023Review
- Proficient Novel Biomarkers Guide Early Detection of Acute Kidney Injury: A Review.Diseases (Basel, Switzerland) · 2022Review
- A slit-diaphragm-associated protein network for dynamic control of renal filtration.Nature communications · 2022Article
- Emerging Biomarkers for Early Detection of Chronic Kidney Disease.Journal of personalized medicine · 2022Review
- Deconvolution of Focal Segmental Glomerulosclerosis Pathophysiology Using Transcriptomics Techniques.Glomerular diseases · 2021Review
- Endoplasmic reticulum-associated degradation is required for nephrin maturation and kidney glomerular filtration function.The Journal of clinical investigation · 2021Article
- Exogenous spermine attenuates diabetic kidney injury in rats by inhibiting AMPK/mTOR signaling pathway.International journal of molecular medicine · 2021Article
- Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome.Acta physiologica (Oxford, England) · 2021Article
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13 authors at 6 institutions in 5 countries.
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Abstract
Podocin is a critical component of the glomerular slit diaphragm, and genetic mutations lead to both familial and sporadic forms of steroid-resistant nephrotic syndrome. In mice, constitutive absence of podocin leads to rapidly progressive renal disease characterized by mesangiolysis and/or mesangial sclerosis and nephrotic syndrome. Using established Cre-loxP technology, we inactivated podocin in the adult mouse kidney in a podocyte-specific manner. Progressive loss of podocin in the glomerulus recapitulated albuminuria, hypercholesterolemia, hypertension, and renal failure seen in nephrotic syndrome in humans. Lesions of FSGS appeared after 4 wk, with subsequent development of diffuse glomerulosclerosis and tubulointerstitial damage. Interestingly, conditional inactivation of podocin at birth resulted in a gradient of glomerular lesions, including mesangial proliferation, demonstrating a developmental stage dependence of renal histologic patterns of injury. The development of significant albuminuria in this model occurred only after early and focal foot process effacement had progressed to diffuse involvement, with complete absence of podocin immunolabeling at the slit diaphragm. Finally, we identified novel potential mediators and perturbed molecular pathways, including cellular proliferation, in the course of progression of renal disease leading to glomerulosclerosis, using global gene expression profiling.
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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.