ArticleJournal of the American Society of Nephrology : JASN2015
Evidence of a Role for Fibroblast Transient Receptor Potential Canonical 3 Ca2+ Channel in Renal Fibrosis.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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.
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Who cites it
38 citing papers in PubMed, 60 citations in OpenAlex.
- Pyrimidinergic calcium signaling links tubular metabolism to fibrosis in kidney disease.Nature communications · 2026Article
- TRPC3 contributes to cyclophosphamide-induced cystitis progression by enhancing bladder fibrosis through activation of the TGF-β/smad pathway.Frontiers in pharmacology · 2025Article
- Calcium signalling and transport in the kidney.Nature reviews. Nephrology · 2024Review
- Sex-specific Stone-forming Phenotype in Mice During Hypercalciuria/Urine Alkalinization.Laboratory investigation; a journal of technical methods and pathology · 2024Article
- TRPC expression in human periodontal ligament cells and the periodontal tissue of periodontitis mice: a preliminary study.Laboratory animal research · 2023Article
- An inactivating human TRPC6 channel mutation without focal segmental glomerulosclerosis.Cellular and molecular life sciences : CMLS · 2023Article
- Histamine activates an intracellular CaFrontiers in cell and developmental biology · 2022Article
- Ion channels as a therapeutic target for renal fibrosis.Frontiers in physiology · 2022Review
- Transient Receptor Potential Channels in the Epithelial-to-Mesenchymal Transition.International journal of molecular sciences · 2021Review
- TRP channels in health and disease at a glance.Journal of cell science · 2021Article
- Polymodal roles of TRPC3 channel in the kidney.Channels (Austin, Tex.) · 2020Review
- CaBritish journal of pharmacology · 2020Review
- Article
- Transient Receptor Potential Channel 6 Knockout Ameliorates Kidney Fibrosis by Inhibition of Epithelial-Mesenchymal Transition.Frontiers in cell and developmental biology · 2020Article
- Huangkui Capsule Ameliorates Renal Fibrosis in a Unilateral Ureteral Obstruction Mouse Model Through TRPC6 Dependent Signaling Pathways.Frontiers in pharmacology · 2020Article
- Role of Transient Receptor Potential Canonical Channels in Heart Physiology and Pathophysiology.Frontiers in cardiovascular medicine · 2020Review
- Advances in Understanding the Effects of Erythropoietin on Renal Fibrosis.Frontiers in medicine · 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
- The Pivotal Role of TRP Channels in Homeostasis and Diseases throughout the Gastrointestinal Tract.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Transient receptor potential canonical (TRPC) Ca(2+)-permeant channels, especially TRPC3, are increasingly implicated in cardiorenal diseases. We studied the possible role of fibroblast TRPC3 in the development of renal fibrosis. In vitro, a macromolecular complex formed by TRPC1/TRPC3/TRPC6 existed in isolated cultured rat renal fibroblasts. However, specific blockade of TRPC3 with the pharmacologic inhibitor pyr3 was sufficient to inhibit both angiotensin II- and 1-oleoyl-2-acetyl-sn-glycerol-induced Ca(2+) entry in these cells, which was detected by fura-2 Ca(2+) imaging. TRPC3 blockade or Ca(2+) removal inhibited fibroblast proliferation and myofibroblast differentiation by suppressing the phosphorylation of extracellular signal-regulated kinase (ERK1/2). In addition, pyr3 inhibited fibrosis and inflammation-associated markers in a noncytotoxic manner. Furthermore, TRPC3 knockdown by siRNA confirmed these pharmacologic findings. In adult male Wistar rats or wild-type mice subjected to unilateral ureteral obstruction, TRPC3 expression increased in the fibroblasts of obstructed kidneys and was associated with increased Ca(2+) entry, ERK1/2 phosphorylation, and fibroblast proliferation. Both TRPC3 blockade in rats and TRPC3 knockout in mice inhibited ERK1/2 phosphorylation and fibroblast activation as well as myofibroblast differentiation and extracellular matrix remodeling in obstructed kidneys, thus ameliorating tubulointerstitial damage and renal fibrosis. In conclusion, TRPC3 channels are present in renal fibroblasts and control fibroblast proliferation, differentiation, and activation through Ca(2+)-mediated ERK signaling. TRPC3 channels might constitute important therapeutic targets for improving renal remodeling in 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.