ArticleJournal of the American Society of Nephrology : JASN2011
TRPC6 enhances angiotensin II-induced albuminuria.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
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Who cites it
79 citing papers in PubMed, 130 citations in OpenAlex.
- The CaPediatric nephrology (Berlin, Germany) · 2025Review
- TRPC6 knockdown-mediated ERK1/2 inactivation alleviates podocyte injury in minimal change disease via upregulating Lon peptidase 1.Renal failure · 2024Article
- Sparsentan improves glomerular hemodynamics, cell functions, and tissue repair in a mouse model of FSGS.JCI insight · 2024Article
- Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024Review
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- The Effects of TRPC6 Knockout in Animal Models of Kidney Disease.Biomolecules · 2022Review
- Transient receptor potential cation channel 6 deficiency leads to increased body weight and metabolic dysfunction.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Recent advances in molecular mechanisms of acute kidney injury in patients with diabetes mellitus.Frontiers in endocrinology · 2022Review
- Transient receptor potential cation channel 6 contributes to kidney injury induced by diabetes and hypertension.American journal of physiology. Renal physiology · 2022Article
- Article
- The glomerular filtration barrier: a structural target for novel kidney therapies.Nature reviews. Drug discovery · 2021Review
- Role of opioid signaling in kidney damage during the development of salt-induced hypertension.Life science alliance · 2020Article
- Polymodal roles of TRPC3 channel in the kidney.Channels (Austin, Tex.) · 2020Review
- The Use of Genomics to Drive Kidney Disease Drug Discovery and Development.Clinical journal of the American Society of Nephrology : CJASN · 2020Review
- Hypertension induces glomerulosclerosis in phospholipase C-ε1 deficiency.American journal of physiology. Renal physiology · 2020Article
- New insight into podocyte slit diaphragm, a therapeutic target of proteinuria.Clinical and experimental nephrology · 2020Review
- Role of Transient Receptor Potential Canonical Channel 6 (TRPC6) in Diabetic Kidney Disease by Regulating Podocyte Actin Cytoskeleton Rearrangement.Journal of diabetes research · 2020Review
- TRPC Channels in Proteinuric Kidney Diseases.Cells · 2019Review
- Tubular injury triggers podocyte dysfunction by β-catenin-driven release of MMP-7.JCI insight · 2019Article
- TRPC6 inactivation does not protect against diabetic kidney disease in streptozotocin (STZ)-treated Sprague-Dawley rats.FASEB bioAdvances · 2019Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
Abstract
Mutations in the canonical transient receptor potential cation channel 6 (TRPC6) are responsible for familial forms of adult onset focal segmental glomerulosclerosis (FSGS). The mechanisms by which TRPC6 mutations cause kidney disease are not well understood. We used TRPC6-deficient mice to examine the function of TRPC6 in the kidney. We found that adult TRPC6-deficient mice had BP and albumin excretion rates similar to wild-type animals. Glomerular histomorphology revealed no abnormalities on both light and electron microscopy. To determine whether the absence of TRPC6 would alter susceptibility to hypertension and renal injury, we infused mice with angiotensin II continuously for 28 days. Although both groups developed similar levels of hypertension, TRPC6-deficient mice had significantly less albuminuria, especially during the early phase of the infusion; this suggested that TRPC6 adversely influences the glomerular filter. We used whole-cell patch-clamp recording to measure cell-membrane currents in primary cultures of podocytes from both wild-type and TRPC6-deficient mice. In podocytes from wild-type mice, angiotensin II and a direct activator of TRPC6 both augmented cell-membrane currents; TRPC6 deficiency abrogated these increases in current magnitude. Our findings suggest that TRPC6 promotes albuminuria, perhaps by promoting angiotensin II-dependent increases in Ca(2+), suggesting that TRPC6 blockade may be therapeutically beneficial in proteinuric kidney 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.