ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
KCNJ2 is Required for NLRP3 Inflammasome Activation That Drives Allergic Airway Inflammation and Remodeling.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Potassium Channels of the Airway Epithelium.Acta physiologica (Oxford, England) · 2026Review
- Lower airway transcriptome signatures in asthma: a newly described cytokine C10orf99 identification.Journal of translational medicine · 2026Article
- KCNJ2 is Required for NLRP3 Inflammasome Activation That Drives Allergic Airway Inflammation and Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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Authors and funding
11 authors.
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Abstract
Airway inflammation and remodeling are cardinal features of asthma pathogenesis. Genome-wide association studies have shown that several SNPs of KCNJ2, a member of the inwardly rectifying potassium channel family, are associated with asthma in patients. However, the role of KCNJ2 in airway inflammation and remodeling in asthma remains unknown. Here, we demonstrate that the Kcnj2 serves as a critical regulator of airway epithelial inflammation and remodeling. KCNJ2 expression is significantly reduced in the airway epithelium of asthmatic patients, which is associated with goblet cell metaplasia and mucus overproduction. Epithelial cell depletion of Kcnj2 attenuates airway inflammation, Th2 inflammatory response, goblet cell metaplasia, and mucus overproduction in the airways of asthmatic mice. In cultured primary airway epithelial cells of asthmatic patients, KCNJ2 inhibition also hampers goblet cell metaplasia, mucus production, and lung epithelial cell-derived alarmins expression. This process appears to be mediated, at least in part, through inhibition of NLRP3 by restricting Ca
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