ArticleCellular and molecular life sciences : CMLS2022
Downregulation of epithelial sodium channel (ENaC) activity in cystic fibrosis cells by epigenetic targeting.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- Epigenetic regulation and chromatin organization in cystic fibrosis airways.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2026Review
- Toward Precision Electrochemical Sensing of CFTR Function in Cystic Fibrosis Models.Analytical chemistry · 2026Article
- Iloprost-loaded inhalable Nano into Micro (NiM) formulations for treating hyper-inflammation in a pre-clinical model of cystic fibrosis airway epithelial cells.Drug delivery and translational research · 2026Article
- Effects ofNutrients · 2025Article
- Curcumin Nanoparticles-related Non-invasive Tumor Therapy, and Cardiotoxicity Relieve.Current medicinal chemistry · 2025Review
- Cystic Fibrosis Modulator Therapies: Bridging Insights from CF to other Membrane Protein Misfolding Diseases.Israel journal of chemistry · 2024Article
- TRPV4 Channel Modulators as Potential Drug Candidates for Cystic Fibrosis.International journal of molecular sciences · 2024Review
- The Impact of Oxidative Stress on the Epigenetics of Fetal Alcohol Spectrum Disorders.Antioxidants (Basel, Switzerland) · 2024Review
- Curcumin and Resveratrol: Nutraceuticals with so Much Potential for Pseudoachondroplasia and Other ER-Stress Conditions.Biomolecules · 2024Review
- SCNN1B regulates the proliferation, migration, and collagen deposition of human lung fibroblasts.In vitro cellular & developmental biology. Animal · 2023Article
- The Epithelial Sodium Channel-An Underestimated Drug Target.International journal of molecular sciences · 2023Review
- Role of epithelial sodium channel-related inflammation in human diseases.Frontiers in immunology · 2023Review
- Gene therapy for cystic fibrosis: Challenges and prospects.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
The pathogenic mechanism of cystic fibrosis (CF) includes the functional interaction of the cystic fibrosis transmembrane conductance regulator (CFTR) protein with the epithelial sodium channel (ENaC). The reduction of ENaC activity may constitute a therapeutic option for CF. This hypothesis was evaluated using drugs that target the protease-dependent activation of the ENaC channel and the transcriptional activity of its coding genes. To this aim we used: camostat, a protease inhibitor; S-adenosyl methionine (SAM), showed to induce DNA hypermethylation; curcumin, known to produce chromatin condensation. SAM and camostat are drugs already clinically used in other pathologies, while curcumin is a common dietary compound. The experimental systems used were CF and non-CF immortalized human bronchial epithelial cell lines as well as human bronchial primary epithelial cells. ENaC activity and SCNN1A, SCNN1B and SCNN1G gene expression were analyzed, in addition to SCNN1B promoter methylation. In both immortalized and primary cells, the inhibition of extracellular peptidases and the epigenetic manipulations reduced ENaC activity. Notably, the reduction in primary cells was much more effective. The SCNN1B appeared to be the best target to reduce ENaC activity, in respect to SCNN1A and SCNN1G. Indeed, SAM treatment resulted to be effective in inducing hypermethylation of SCNN1B gene promoter and in lowering its expression. Importantly, CFTR expression was unaffected, or even upregulated, after treatments. These results open the possibility of CF patients' treatment by epigenetic targeting.
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