ArticleJournal of molecular medicine (Berlin, Germany)2018
Trpc6 inactivation confers protection in a model of severe nephrosis in rats.
Article in Journal of molecular medicine (Berlin, Germany), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Focus on podocytes: diabetic kidney disease and renal fibrosis - a global bibliometric analysis (2000-2024).Frontiers in pharmacology · 2024Pooled it
- Preclinical approaches to studying liver and kidney fibrosis: models and methodologies.Frontiers in pharmacology · 2026Review
- The critical role of ion channels in kidney disease: perspective from AKI and CKD.Renal failure · 2025Review
- TRPC6 effects on albumin permeation, nephrin shedding, and apoptosis in podocytes: Role of calcineurin and metalloproteases.Physiological reports · 2025Article
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- A Putative Role for TRPC6 in Immune-Mediated Kidney Injury.International journal of molecular sciences · 2023Review
- An inactivating human TRPC6 channel mutation without focal segmental glomerulosclerosis.Cellular and molecular life sciences : CMLS · 2023Article
- The small GTPase regulatory protein Rac1 drives podocyte injury independent of cationic channel protein TRPC5.Kidney international · 2023Article
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- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Role of ion channels in the mechanism of proteinuria (Review).Experimental and therapeutic medicine · 2023Review
- Transient receptor potential canonical 6 knockdown ameliorated diabetic kidney disease by inhibiting nuclear factor of activated T cells 2 expression in glomerular mesangial cells.Renal failure · 2022Article
- The Effects of TRPC6 Knockout in Animal Models of Kidney Disease.Biomolecules · 2022Review
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- Isoflavone daidzein ameliorates renal dysfunction and fibrosis in a postmenopausal rat model: Intermediation of angiotensin AT1 and Mas receptors and microRNAs 33a and 27a.Iranian journal of basic medical sciences · 2022Article
- TRPC6 Inactivation Reduces Albuminuria Induced by Protein Overload in Sprague Dawley Rats.Cells · 2022Article
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- Repurposing Riociguat to Target a Novel Paracrine Nitric Oxide-TRPC6 Pathway to Prevent Podocyte Injury.International journal of molecular sciences · 2021Article
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Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in canonical transient receptor potential-6 (TRPC6) channels give rise to rare familial forms of focal and segmental glomerulosclerosis (FSGS). Here we examined a possible role for TRPC6 in the progression of chronic puromycin aminonucleoside (PAN) nephrosis in Sprague-Dawley rats, a classic model of acquired nephrotic syndromes. We used CRISPR/Cas9 technology to delete a 239-bp region within exon 2 of the Trpc6 gene (Trpc6 KEY MESSAGES: We examined aminonucleoside nephrosis in rats with wild type and inactivated TRPC6. TRPC6 channels were inactivated by CRISPR/Cas9 editing of the Trpc6 gene. TRPC6 inactivation reduced albuminuria in the chronic but not the acute phase. TRPC6 inactivation reduced glomerulosclerosis and ultrastructural changes. TRPC6 inactivation also reduced interstitial changes and renal fibrosis.
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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.