ArticleJournal of the American Society of Nephrology : JASN2016
Synaptopodin Limits TRPC6 Podocyte Surface Expression and Attenuates Proteinuria.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 55 citations in OpenAlex.
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- Xanthohumol exerts protective function on adriamycin-induced podocyte injury.European journal of nutrition · 2025Article
- Diagnostic value of the correlation between urinary MDM2 and podocyte mitotic catastrophe in diabetic kidney disease.Diabetology & metabolic syndrome · 2025Article
- TRPC6-targeted dexamethasone nanobubbles with ultrasound-guided theranostics for adriamycin-induced nephropathy.Journal of nanobiotechnology · 2025Article
- Umbilical Cord Mesenchymal Stem Cells Attenuate Podocyte Injury in Diabetic Nephropathy Rats by Inhibiting Angpltl4/IntegrinJournal of diabetes research · 2025Article
- Podocyte cell-specificPhysiological genomics · 2024Article
- Genetically conditioned interaction among microRNA-155, alpha-klotho, and intra-renal RAS in male rats: Link to CKD progression.Physiological reports · 2024Article
- A simple protocol to establish a conditionally immortalized mouse podocyte cell line.Scientific reports · 2024Article
- "Qi Nan" agarwood restores podocyte autophagy in diabetic kidney disease by targeting EGFR signaling pathway.Chinese medicine · 2024Article
- 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
- Klotho Stabilizes the Podocyte Actin Cytoskeleton in Idiopathic Membranous Nephropathy through Regulating the TRPC6/CatL Pathway.American journal of nephrology · 2024Article
- Nephrotic syndrome: pathophysiology and consequences.Journal of nephrology · 2023Review
- Abnormal Lipoproteins Trigger Oxidative Stress-Mediated Apoptosis of Renal Cells in LCAT Deficiency.Antioxidants (Basel, Switzerland) · 2023Article
- Store-operated CaExperimental biology and medicine (Maywood, N.J.) · 2023Review
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Upregulation of OASIS/CREB3L1 in podocytes contributes to the disturbance of kidney homeostasis.Communications biology · 2022Article
- Tetrandrine Attenuates Podocyte Injury by Inhibiting TRPC6-Mediated RhoA/ROCK1 Pathway.Analytical cellular pathology (Amsterdam) · 2022Article
- Article
- The Pathophysiologic Role of Gelsolin in Chronic Kidney Disease: Focus on Podocytes.International journal of molecular sciences · 2021Article
- Renal cell markers: lighthouses for managing renal diseases.American journal of physiology. Renal physiology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
Abstract
Gain-of-function mutations of classic transient receptor potential channel 6 (TRPC6) were identified in familial FSGS, and increased expression of wild-type TRPC6 in glomeruli is observed in several human acquired proteinuric diseases. Synaptopodin, an actin binding protein that is important in maintaining podocyte function, is downregulated in various glomerular diseases. Here, we investigated whether synaptopodin maintains podocyte function by regulating podocyte surface expression and activity of TRPC6. We show indirect interaction and nonrandom association of synaptopodin and TRPC6 in podocytes. Knockdown of synaptopodin in cultured mouse podocytes increased the expression of TRPC6 at the plasma membrane, whereas overexpression of synaptopodin decreased it. Mechanistically, synaptopodin-dependent TRPC6 surface expression required functional actin and microtubule cytoskeletons. Overexpression of wild-type or FSGS-inducing mutant TRPC6 in synaptopodin-depleted podocytes enhanced TRPC6-mediated calcium influx and induced apoptosis. In vivo, knockdown of synaptopodin also caused increased podocyte surface expression of TRPC6. Administration of cyclosporin A, which stabilizes synaptopodin, reduced LPS-induced proteinuria significantly in wild-type mice but to a lesser extent in TRPC6 knockout mice. Furthermore, administration of cyclosporin A reversed the LPS-induced increase in podocyte surface expression of TRPC6 in wild-type mice. Our findings suggest that alteration in synaptopodin levels under disease conditions may modify intracellular TRPC6 channel localization and activity, which further contribute to podocyte dysfunction. Reducing TRPC6 surface levels may be a new approach to restoring podocyte function.
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