ArticleJCI insight2020
Lack of Kcnn4 improves mucociliary clearance in muco-obstructive lung disease.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Potassium Channels of the Airway Epithelium.Acta physiologica (Oxford, England) · 2026Review
- Succinate Chemosensing Induces Cystic Fibrosis Transmembrane Conductance Regulator-dependent Airway Clearance that Is Impaired in Cystic Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- Cyclosporine A Accelerates Neurorecovery Transcriptional Trajectory in a Swine Model of Diffuse Traumatic Brain Injury.International journal of molecular sciences · 2025Article
- Exploring the Mechanisms of Lijin Fang on Treg/Th17 Cell Imbalance in COPD Based on Network Pharmacology.International journal of chronic obstructive pulmonary disease · 2025Article
- TRPV4 Channel Modulators as Potential Drug Candidates for Cystic Fibrosis.International journal of molecular sciences · 2024Review
- Pseudomonas aeruginosa senses and responds to epithelial potassium flux via Kdp operon to promote biofilm.PLoS pathogens · 2024Article
- Function of KvLQT1 potassium channels in a mouse model of bleomycin-induced acute lung injury.Frontiers in physiology · 2024Article
- Epigenetic regulation of macrophage activation in chronic obstructive pulmonary disease.Frontiers in immunology · 2024Review
- KBiomedicines · 2023Review
- Physiology and pathophysiology of human airway mucus.Physiological reviews · 2022Review
- Inhibition of the sodium-dependent HCOeLife · 2022Article
- CLCA1 Regulates Airway Mucus Production and Ion Secretion Through TMEM16A.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Airway mucociliary clearance (MCC) is the main mechanism of lung defense keeping airways free of infection and mucus obstruction. Airway surface liquid volume, ciliary beating, and mucus are central for proper MCC and critically regulated by sodium absorption and anion secretion. Impaired MCC is a key feature of muco-obstructive diseases. The calcium-activated potassium channel KCa.3.1, encoded by Kcnn4, participates in ion secretion, and studies showed that its activation increases Na+ absorption in airway epithelia, suggesting that KCa3.1-induced hyperpolarization was sufficient to drive Na+ absorption. However, its role in airway epithelium is not fully understood. We aimed to elucidate the role of KCa3.1 in MCC using a genetically engineered mouse. KCa3.1 inhibition reduced Na+ absorption in mouse and human airway epithelium. Furthermore, the genetic deletion of Kcnn4 enhanced cilia beating frequency and MCC ex vivo and in vivo. Kcnn4 silencing in the Scnn1b-transgenic mouse (Scnn1btg/+), a model of muco-obstructive lung disease triggered by increased epithelial Na+ absorption, improved MCC, reduced Na+ absorption, and did not change the amount of mucus but did reduce mucus adhesion, neutrophil infiltration, and emphysema. Our data support that KCa3.1 inhibition attenuated muco-obstructive disease in the Scnn1btg/+ mice. K+ channel modulation may be a therapeutic strategy to treat muco-obstructive lung diseases.
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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.