ReviewMolecular bioSystems2009
Assessment of the CFTR and ENaC association.
Review in Molecular bioSystems, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
82 citing papers in PubMed, 136 citations in OpenAlex.
- 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
- Human Nasal and Bronchial Epithelium in Cystic Fibrosis: Differences in Expression of Airway pH Regulatory Proteins.Pediatric pulmonology · 2026Article
- Acquired cystic fibrosis transmembrane conductance regulator dysfunction.Pflugers Archiv : European journal of physiology · 2025Review
- Respiratory Ciliary Beat Frequency in COPD: Balancing Oxidative Stress and Pharmacological Treatment.Antioxidants (Basel, Switzerland) · 2025Review
- Cystic Fibrosis Modulator Therapies: Bridging Insights from CF to other Membrane Protein Misfolding Diseases.Israel journal of chemistry · 2024Article
- Review
- The effect of triple CFTR modulator therapy and azithromycin on ion channels and inflammation in cystic fibrosis.ERJ open research · 2024Article
- Cystic Fibrosis: A Journey through Time and Hope.International journal of molecular sciences · 2024Review
- Inflammation in the COVID-19 airway is due to inhibition of CFTR signaling by the SARS-CoV-2 spike protein.Scientific reports · 2024Article
- Article
- CFTR dysfunction leads to defective bacterial eradication on cystic fibrosis airways.Frontiers in physiology · 2024Review
- Signaling Roleplay between Ion Channels during Mammalian Sperm Capacitation.Biomedicines · 2023Review
- A Proteomic Survey of the Cystic Fibrosis Transmembrane Conductance Regulator Surfaceome.International journal of molecular sciences · 2023Review
- Bioelectric regulation of intestinal stem cells.Trends in cell biology · 2023Review
- Skin-Interfaced Wearable Sweat Sensors for Precision Medicine.Chemical reviews · 2023Review
- A NovelJournal of clinical research in pediatric endocrinology · 2022Article
- A Review on the Role of Bicarbonate and Proton Transporters during Sperm Capacitation in Mammals.International journal of molecular sciences · 2022Review
- Biphasic regulation of CFTR expression by ENaC in epithelial cells: The involvement of CaFrontiers in cell and developmental biology · 2022Article
- The Interplay between the Unfolded Protein Response, Inflammation and Infection in Cystic Fibrosis.Cells · 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
22 more citing papers are in PubMed but not listed here.
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
Cystic fibrosis (CF) is one of the most common lethal genetic disorders. It results primarily from mutations in the cystic fibrosis transmembrane conductance regulator (cftr) gene. These mutations cause inadequate functioning of CFTR, which in turn leads to the severe disruption of transport function in several epithelia across various organs. Affected organs include the sweat glands, the intestine, and the reproductive system, with the most devastating consequences due to the effects of the disease on airways. Despite aggressive treatment, gradual lung failure is the major life limiting factor in patients with CF. Understanding of the exact manner by which defects in the CFTR lead to lung failure is thus critical. In the CF airway, decreased chloride secretion and increased salt absorption is observed. The decreased chloride secretion appears to be a direct consequence of defective CFTR; however, the increased salt absorption is believed to result from the failure of CFTR to restrict salt absorption through a sodium channel named the epithelial Na(+) channel, ENaC. The mechanism by which CFTR modulates the function of ENaC proteins is still obscure and somewhat controversial. In this short review we will focus on recent findings of a possible direct CFTR and ENaC association.
Indexed as
Identifiers
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.