ReviewAmerican journal of physiology. Renal physiology2010
TRPC6 channels and their binding partners in podocytes: role in glomerular filtration and pathophysiology.
Review in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
85 citing papers in PubMed, 164 citations in OpenAlex.
- Activation of BKCurrent issues in molecular biology · 2026Article
- Network pharmacology andArchives of medical science : AMS · 2026Article
- Structural and functional insights of the podocyte slit diaphragm complex.Tissue barriers · 2026Review
- Genotype-phenotype correlations and clinical outcomes of genetic TRPC6 podocytopathies.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Observational
- The critical role of ion channels in kidney disease: perspective from AKI and CKD.Renal failure · 2025Review
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- Natural History and Clinicopathological Associations of TRPC6-Associated Podocytopathy.Journal of the American Society of Nephrology : JASN · 2025Article
- The roles of TRPC6 in renal tubular disorders: a narrative review.Renal failure · 2024Review
- Novel Pathogenic Mutation of P209L in TRPC6 Gene Causes Adult Focal Segmental Glomerulosclerosis.Biochemical genetics · 2024Article
- Review
- Sparsentan improves glomerular hemodynamics, cell functions, and tissue repair in a mouse model of FSGS.JCI insight · 2024Article
- Proteome-scale characterisation of motif-based interactome rewiring by disease mutations.Molecular systems biology · 2024Article
- Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024Review
- The key mediator of diabetic kidney disease: Potassium channel dysfunction.Genes & diseases · 2024Review
- Article
- Biophysical characterization and insights into the oligomeric nature of CD2-associated protein.International journal of biochemistry and molecular biology · 2024Article
- Immune podocytes in the immune microenvironment of lupus nephritis (Review).Molecular medicine reports · 2023Review
- Podocyte protease activated receptor 1 stimulation in mice produces focal segmental glomerulosclerosis mirroring human disease signaling events.Kidney international · 2023Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Loss or dysfunction of podocytes is a major cause of glomerular kidney disease. Several genetic forms of glomerular disease are caused by mutations in genes that encode structural elements of the slit diaphragm or the underlying cytoskeleton of podocyte foot processes. The recent discovery that gain-of-function mutations in Ca(2+)-permeable canonical transient receptor potential-6 channels (TRPC6) underlie a subset of familial forms of focal segmental glomerulosclerosis (FSGS) has focused attention on the basic cellular physiology of podocytes. Several recent studies have examined the role of Ca(2+) dynamics in normal podocyte function and their possible contributions to glomerular disease. This review summarizes the properties of TRPC6 and related channels, focusing on their permeation and gating properties, the nature of mutations associated with familial FSGS, and the role of TRPC channels in podocyte cell biology as well as in glomerular pathophysiology. TRPC6 interacts with several proteins in podocytes, including essential slit diaphragm proteins and mechanosensitive large-conductance Ca(2+)-activated K(+) channels. The signaling dynamics controlling ion channel function and localization in podocytes appear to be quite complex.
Indexed as
Identifiers
What OpenQuestion holds
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.