ArticlePloS one2013
The K+ channel KCa3.1 as a novel target for idiopathic pulmonary fibrosis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 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
31 citing papers in PubMed, 53 citations in OpenAlex.
- Senicapoc in Patients with Idiopathic Pulmonary Fibrosis or Other Progressive Fibrotic Interstitial Lung Diseases: Protocol for a Randomised, Double-Blind, Placebo-Controlled, Multicentre Phase II Trial.Diagnostics (Basel, Switzerland) · 2026Article
- The KCa3.1 KCells · 2026Review
- Comparison of the Transcriptomic Signatures of Skin and Lung Fibroblasts from Patients with Systemic Sclerosis.Fibrosis (Hong Kong, China) · 2026Article
- The role and mechanism of vascular wall cell ion channels in vascular fibrosis remodeling.Channels (Austin, Tex.) · 2024Review
- Regulation of myofibroblast dedifferentiation in pulmonary fibrosis.Respiratory research · 2024Review
- Precision Medicine in Erythropoietin Deficiency and Treatment Resistance: A Novel Approach to Management of Anaemia in Chronic Kidney Disease.Current issues in molecular biology · 2023Review
- KBiomedicines · 2023Review
- Harnessing the Role of HDAC6 in Idiopathic Pulmonary Fibrosis: Design, Synthesis, Structural Analysis, and Biological Evaluation of Potent Inhibitors.Journal of medicinal chemistry · 2021Article
- ATP-evoked intracellular CaJournal of neuroinflammation · 2021Article
- Evaluation of Pirfenidone and Nintedanib in a Human Lung Model of Fibrogenesis.Frontiers in pharmacology · 2021Article
- Increased Levels of ER Stress and Apoptosis in a Sheep Model for Pulmonary Fibrosis Are Alleviated byCanadian respiratory journal · 2021Article
- CaBritish journal of pharmacology · 2020Review
- The Role of KCNMB1 and BK Channels in Myofibroblast Differentiation and Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2020Article
- Ion Channels Orchestrate Pancreatic Ductal Adenocarcinoma Progression and Therapy.Frontiers in pharmacology · 2020Review
- KScientific reports · 2019Article
- Validation of antibodies for the specific detection of human TRPA1.Scientific reports · 2019Article
- Cardiac fibroblasts : Active players in (atrial) electrophysiology?Herzschrittmachertherapie & Elektrophysiologie · 2018Review
- NPPB modulates apoptosis, proliferation, migration and extracellular matrix synthesis of conjunctival fibroblasts by inhibiting PI3K/AKT signaling.International journal of molecular medicine · 2018Article
- Blockade of KCa3.1: A novel target to treat TGF-β1 induced conjunctival fibrosis.Experimental eye research · 2018Article
- A model of human lung fibrogenesis for the assessment of anti-fibrotic strategies in idiopathic pulmonary fibrosis.Scientific reports · 2018Article
Corrections and comments
- Erratum issuedRoach, Katy Morgan [corrected to Roach, Katy M]
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a common, progressive and invariably lethal interstitial lung disease with no effective therapy. We hypothesised that K(Ca)3.1 K(+) channel-dependent cell processes contribute to IPF pathophysiology.
methodsK(Ca)3.1 expression in primary human lung myofibroblasts was examined using RT-PCR, western blot, immunofluorescence and patch-clamp electrophysiology. The role of K(Ca)3.1 channels in myofibroblast proliferation, wound healing, collagen secretion and contraction was examined using two specific and distinct K(Ca)3.1 blockers (TRAM-34 and ICA-17043 [Senicapoc]).
resultsBoth healthy non fibrotic control and IPF-derived human lung myofibroblasts expressed K(Ca)3.1 channel mRNA and protein. K(Ca)3.1 ion currents were elicited more frequently and were larger in IPF-derived myofibroblasts compared to controls. K(Ca)3.1 currents were increased in myofibroblasts by TGFβ1 and basic FGF. K(Ca)3.1 was expressed strongly in IPF tissue. K(Ca)3.1 pharmacological blockade attenuated human myofibroblast proliferation, wound healing, collagen secretion and contractility in vitro, and this was associated with inhibition of TGFβ1-dependent increases in intracellular free Ca(2+).
conclusionsK(Ca)3.1 activity promotes pro-fibrotic human lung myofibroblast function. Blocking K(Ca)3.1 may offer a novel approach to treating IPF with the potential for rapid translation to the clinic.
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