ReviewCold Spring Harbor perspectives in medicine2013
New pulmonary therapies directed at targets other than CFTR.
Review in Cold Spring Harbor perspectives in medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 17 citations in OpenAlex.
- In Vitro Models for Studying Respiratory Host-Pathogen Interactions.Advanced biology · 2021Review
- Review
- The epithelial sodium channel (ENaC) as a therapeutic target for cystic fibrosis.Current opinion in pharmacology · 2018Review
- The Epithelial Sodium Channel (αENaC) Is a Downstream Therapeutic Target of ASCL1 in Pulmonary Neuroendocrine Tumors.Translational oncology · 2018Article
- The Epithelial Sodium Channel Is a Modifier of the Long-Term Nonprogressive Phenotype Associated with F508del CFTR Mutations.American journal of respiratory cell and molecular biology · 2017Article
- Role of CFTR in epithelial physiology.Cellular and molecular life sciences : CMLS · 2017Review
- Inhibitors of pendrin anion exchange identified in a small molecule screen increase airway surface liquid volume in cystic fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Mechanism of allosteric activation of TMEM16A/ANO1 channels by a commonly used chloride channel blocker.British journal of pharmacology · 2016Article
- Inhibition of ENaC by endothelin-1.Vitamins and hormones · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our current understanding of the pathogenesis of cystic fibrosis (CF) lung disease stresses the importance of the physical and chemical properties of the airway surface liquid (ASL). In particular, the loss of cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel function in CF reduces the volume and fluidity of the ASL, thus impairing mucociliary clearance and innate antimicrobial mechanisms. Besides direct approaches to restoring mutant CFTR function, alternative therapeutic strategies may also be considered to correct the basic defect of impaired salt and water transport. Such alternative strategies are focused on the restoration of mucociliary transport by (1) reducing sodium and fluid absorption by inhibiting the ENaC channel; (2) activating alternative chloride channels; and (3) increasing airway surface hydration with osmotic agents. Therapeutic approaches directed at targets other than CFTR are attractive because they are potentially useful to all patients irrespective of their genotype. Clinical trials are underway to test the efficacy of these approaches.
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.