ArticlePloS one2010
Podocyte-specific overexpression of wild type or mutant trpc6 in mice is sufficient to cause glomerular disease.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 129 citations in OpenAlex.
- Treatment outcomes and ongoing pediatric trials in steroid-resistant nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2026Review
- Emerging genetic mechanisms of glomerular proteinuria: a podocyte-centered multi-layer network perspective.Frontiers in genetics · 2026Review
- Podocyte-targeted therapies - progress and future directions.Nature reviews. Nephrology · 2024Review
- Experimental models for preclinical research in kidney disease.Zoological research · 2024Review
- Sparsentan improves glomerular hemodynamics, cell functions, and tissue repair in a mouse model of FSGS.JCI insight · 2024Article
- Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024Review
- CD36-mediated podocyte lipotoxicity promotes foot process effacement.Open medicine (Warsaw, Poland) · 2024Article
- The small GTPase regulatory protein Rac1 drives podocyte injury independent of cationic channel protein TRPC5.Kidney international · 2023Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Current understanding of the molecular mechanisms of circulating permeability factor in focal segmental glomerulosclerosis.Frontiers in immunology · 2023Review
- The Effects of TRPC6 Knockout in Animal Models of Kidney Disease.Biomolecules · 2022Review
- Monogenic focal segmental glomerulosclerosis: A conceptual framework for identification and management of a heterogeneous disease.American journal of medical genetics. Part C, Seminars in medical genetics · 2022Review
- TRPC6 Inactivation Reduces Albuminuria Induced by Protein Overload in Sprague Dawley Rats.Cells · 2022Article
- The role of TRPC6 channel in chronic kidney disease.American journal of physiology. Renal physiology · 2022Article
- Article
- Mutational landscape of TRPC6, WT1, LMX1B, APOL1, PTPRO, PMM2, LAMB2 and WT1 genes associated with Steroid resistant nephrotic syndrome.Molecular biology reports · 2021Article
- Deconvolution of Focal Segmental Glomerulosclerosis Pathophysiology Using Transcriptomics Techniques.Glomerular diseases · 2021Review
- The glomerular filtration barrier: a structural target for novel kidney therapies.Nature reviews. Drug discovery · 2021Review
- Tacrolimus Protects Podocytes from Apoptosis via Downregulation of TRPC6 in Diabetic Nephropathy.Journal of diabetes research · 2021Article
- Nephrotoxicity and genotoxicity of silver nanoparticles in juvenile rats and possible mechanisms of action.Arhiv za higijenu rada i toksikologiju · 2020Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Mutations in the TRPC6 calcium channel (Transient receptor potential channel 6) gene have been associated with familiar forms of Focal and Segmental Glomerulosclerosis (FSGS) affecting children and adults. In addition, acquired glomerular diseases are associated with increased expression levels of TRPC6. However, the exact role of TRPC6 in the pathogenesis of FSGS remains to be elucidated. In this work we describe the generation and phenotypic characterization of three different transgenic mouse lines with podocyte-specific overexpression of the wild type or any of two mutant forms of Trpc6 (P111Q and E896K) previously related to FSGS. Consistent with the human phenotype a non-nephrotic range of albuminuria was detectable in almost all transgenic lines. The histological analysis demonstrated that the transgenic mice developed a kidney disease similar to human FSGS. Differences of 2-3 folds in the presence of glomerular lesions were found between the non transgenic and transgenic mice expressing Trpc6 in its wild type or mutant forms specifically in podocytes. Electron microscopy of glomerulus from transgenic mice showed extensive podocyte foot process effacement. We conclude that overexpression of Trpc6 (wild type or mutated) in podocytes is sufficient to cause a kidney disease consistent with FSGS. Our results contribute to reinforce the central role of podocytes in the etiology of FSGS. These mice constitute an important new model in which to study future therapies and outcomes of this complex disease.
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Registered trials
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.