ReviewThe Journal of physiology2013
Does epithelial sodium channel hyperactivity contribute to cystic fibrosis lung disease?
Review in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 92 citations in OpenAlex.
- Understanding Nasal Polyposis: The Roles of Ion Channels, Inflammation, Ionocytes, and Prostaglandin E2-The IJournal of clinical medicine · 2026Article
- Taste Receptor Activation in Tracheal Brush Cells by Denatonium Modulates ENaC Channels via CaCells · 2022Article
- Transmembrane serine protease 2 (TMPRSS2) proteolytically activates the epithelial sodium channel (ENaC) by cleaving the channel's γ-subunit.The Journal of biological chemistry · 2022Article
- Biphasic regulation of CFTR expression by ENaC in epithelial cells: The involvement of CaFrontiers in cell and developmental biology · 2022Article
- Article
- Review
- Perspectives on the translation of in-vitro studies to precision medicine in Cystic Fibrosis.EBioMedicine · 2021Review
- Association of cystic fibrosis transmembrane conductance regulator with epithelial sodium channel subunits carrying Liddle's syndrome mutations.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Trypsin-Like Proteases and Their Role in Muco-Obstructive Lung Diseases.International journal of molecular sciences · 2021Review
- Cystic fibrosis-related diabetes and lung disease: an update.European respiratory review : an official journal of the European Respiratory Society · 2021Review
- IRE1α Is a Therapeutic Target for Cystic Fibrosis Airway Inflammation.International journal of molecular sciences · 2021Article
- Is the ENaC Dysregulation in CF an Effect of Protein-Lipid Interaction in the Membranes?International journal of molecular sciences · 2021Review
- Downregulation of epithelial sodium channel (ENaC) activity in human airway epithelia after low temperature incubation.BMJ open respiratory research · 2021Article
- New Therapeutic Approaches in Cystic Fibrosis.Turkish journal of pharmaceutical sciences · 2020Article
- Dysregulated signalling pathways in innate immune cells with cystic fibrosis mutations.Cellular and molecular life sciences : CMLS · 2020Review
- Capsaicin-Loaded Chitosan Nanocapsules for wtCFTR-mRNA Delivery to a Cystic Fibrosis Cell Line.Biomedicines · 2020Article
- ENaC regulation by phospholipids and DGK explained through mathematical modeling.Scientific reports · 2020Article
- Gene Therapy for Cystic Fibrosis: Progress and Challenges of Genome Editing.International journal of molecular sciences · 2020Review
- Pharmacological modulation of mitochondrial calcium uniporter controls lung inflammation in cystic fibrosis.Science advances · 2020Article
- High-mobility group box-1 increases epithelial sodium channel activity and inflammation via the receptor for advanced glycation end products.American journal of physiology. Cell physiology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Airway epithelia absorb Na+ through the epithelial Na+ channel (ENaC) and secrete Cl- through the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel. This balance maintains sufficient airway surface liquid hydration to permit efficient mucus clearance, which is needed to maintain sterility of the lung. Cystic fibrosis (CF) is a common autosomal recessive inherited disease caused by mutations in the CFTR gene that lead to the reduction or elimination of the CFTR protein. CF is a multi-organ disease that affects epithelia lining the intestines, lungs, pancreas, sweat ducts and vas deferens, among others. CF lungs are characterized by viscous, dehydrated mucus, persistent neutrophilia and chronic infections. ENaC is negatively regulated by CFTR and, in patients with CF, the absence of CFTR results in a double hit of reduced Cl-/HCO3- and H2O secretion as well as ENaC hyperactivity and increased Na+ and H2O absorption. Together, these effects are hypothesized to trigger mucus dehydration, resulting in a failure to clear mucus. Rehydrating CF mucus has become a recent clinical focus and yields important end-points for clinical trials. However, while ENaC hyperactivity in CF airways has been detected in vivo and in vitro, recent data have brought the role of ENaC in CF lung disease pathogenesis into question. This review will focus on our current understanding of the contribution of ENaC to CF pathogenesis.
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What OpenQuestion holds
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.