ReviewCurrent opinion in pharmacology2018
The epithelial sodium channel (ENaC) as a therapeutic target for cystic fibrosis.
Review in Current opinion in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed.
- Efficacy and safety of inhaled ENaC inhibitor BI 1265162 in patients with cystic fibrosis: BALANCE-CF 1, a randomised, phase II study.The European respiratory journal · 2022Trial
- Amiloride mitigates respiratory distress caused by WFDC2 deficiency via inhibiting the epithelial sodium channel.Nature communications · 2026Article
- Inhalable gene and RNA therapy for cystic fibrosis: perspectives and progress in clinical development.Nanomedicine (London, England) · 2026Review
- Article
- ENaC contributes to macrophage dysfunction in cystic fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Mucins and Their Roles in Asthma.Immunological reviews · 2025Review
- Global functional genomics reveals GRK5 as a cystic fibrosis therapeutic target synergistic with current modulators.iScience · 2025Article
- Randomised, phase 1/2a trial of ION-827359, an antisense oligonucleotide inhibitor of ENaC.ERJ open research · 2024Article
- Emerging cell and molecular targets for treating mucus hypersecretion in asthma.Allergology international : official journal of the Japanese Society of Allergology · 2024Review
- Effects of CFTR-ENaC on spinal cord edema after spinal cord injury.Open medicine (Warsaw, Poland) · 2024Article
- Muco-Obstructive Lung Disease: A Systematic Review.Cureus · 2023Review
- Hormonal regulation of non-cystic fibrosis transmembrane conductance regulator ion channels in the endocervix.F&S science · 2023Article
- The Epithelial Sodium Channel-An Underestimated Drug Target.International journal of molecular sciences · 2023Review
- Molecular targets for cystic fibrosis and therapeutic potential of monoclonal antibodies.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022Review
- Airway surface hyperviscosity and defective mucociliary transport by IL-17/TNF-α are corrected by β-adrenergic stimulus.JCI insight · 2022Article
- Preclinical evaluation of the epithelial sodium channel inhibitor AZD5634 and implications on human translation.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Physiology and pathophysiology of human airway mucus.Physiological reviews · 2022Review
- Oligonucleotide-based therapies for cystic fibrosis.Current opinion in pharmacology · 2022Review
- Small-molecule eRF3a degraders rescue CFTR nonsense mutations by promoting premature termination codon readthrough.The Journal of clinical investigation · 2022Article
- Functional evaluation of the cystic fibrosis transmembrane conductance regulator in the endocervix†.Biology of reproduction · 2022Article
Corrections and comments
- Commented on byEditorial.2018
Authors and funding
4 authors.
Funding
Abstract
Cystic fibrosis (CF) is a monogenic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. CFTR dysfunction is characterized by abnormal mucociliary transport due to a dehydrated airway surface liquid (ASL) and hyperviscous mucus, among other pathologies of host defense. ASL depletion is caused by the absence of CFTR mediated chloride secretion along with continued activity of the epithelial sodium channel (ENaC) activity, which can also be affected by CFTR mediated anion conductance. Therefore, ENaC has been proposed as a therapeutic target to ameliorate ASL dehydration and improve mucus transport. Inhibition of ENaC has been shown to restore ASL hydration and enhance mucociliary transport in induced models of CF lung disease. To date, no therapy inhibiting ENaC has successfully translated to clinical efficacy, in part due to concerns regarding off-target effects, systemic exposure, durability of effect, and adverse effects. Recent efforts have been made to develop novel, rationally designed therapeutics to produce-specific, long-lasting inhibition of ENaC activity in the airways while simultaneously minimizing off target fluid transport effects, systemic exposure and side effects. Such approaches comprise next-generation small molecule direct inhibitors, indirect channel-activating protease inhibitors, synthetic peptide analogs, and oligonucleotide-based therapies. These novel therapeutics represent an exciting step forward in the development of ENaC-directed therapies for CF.
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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.