ReviewCell death and differentiation2017
Strategies for the etiological therapy of cystic fibrosis.
Review in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 57 citations in OpenAlex.
- APPLICATION OF QUANTILE DISCRETIZATION AND BAYESIAN NETWORK ANALYSIS TO PUBLICLY AVAILABLE CYSTIC FIBROSIS DATA SETS.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2024Article
- The Effect of Complex Alleles of theInternational journal of molecular sciences · 2023Review
- A comprehensive review of cystic fibrosis in Africa and Asia.Saudi journal of biological sciences · 2023Review
- Virtual Drug Repositioning as a Tool to Identify Natural Small Molecules That Synergize with Lumacaftor in F508del-CFTR Binding and Rescuing.International journal of molecular sciences · 2022Article
- Beyond Mendelian Inheritance: Genetic Buffering and Phenotype Variability.Phenomics (Cham, Switzerland) · 2022Review
- Anakinra restores cellular proteostasis by coupling mitochondrial redox balance to autophagy.The Journal of clinical investigation · 2022Article
- Exon-skipping antisense oligonucleotides for cystic fibrosis therapy.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Distinctive metabolic profiles between Cystic Fibrosis mutational subclasses and lung function.Metabolomics : Official journal of the Metabolomic Society · 2021Article
- The Multifaceted Roles of MicroRNAs in Cystic Fibrosis.Diagnostics (Basel, Switzerland) · 2020Review
- Complex interplay between autophagy and oxidative stress in the development of pulmonary disease.Redox biology · 2020Review
- Cell-Based Therapeutic Approaches for Cystic Fibrosis.International journal of molecular sciences · 2020Review
- Disorders of FZ-CRD; insights towards FZ-CRD folding and therapeutic landscape.Molecular medicine (Cambridge, Mass.) · 2019Review
- Cystic fibrosis transmembrane conductance regulator (CFTR) and autophagy: hereditary defects in cystic fibrosisOncotarget · 2019Review
- Cystic Fibrosis Mutation Spectrum in North Macedonia: A Step Toward Personalized Therapy.Balkan journal of medical genetics : BJMG · 2019Article
- Article
- Autophagy suppresses the pathogenic immune response to dietary antigens in cystic fibrosis.Cell death & disease · 2019Article
- Therapeutic modulation of autophagy: which disease comes first?Cell death and differentiation · 2019Review
- Defective proteostasis in celiac disease as a new therapeutic target.Cell death & disease · 2019Review
- Stem cell-based Lung-on-Chips: The best of both worlds?Advanced drug delivery reviews · 2019Review
- Adapting Proteostasis and Autophagy for Controlling the Pathogenesis of Cystic Fibrosis Lung Disease.Frontiers in pharmacology · 2019Review
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 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Etiological therapies aim at repairing the underlying cause of cystic fibrosis (CF), which is the functional defect of the cystic fibrosis transmembrane conductance regulator (CFTR) protein owing to mutations in the CFTR gene. Among these, the F508del CFTR mutation accounts for more than two thirds of CF cases worldwide. Two somehow antinomic schools of thought conceive CFTR repair in a different manner. According to one vision, drugs should directly target the mutated CFTR protein to increase its plasma membrane expression (correctors) or improve its ion transport function (potentiators). An alternative strategy consists in modulating the cellular environment and proteostasis networks in which the mutated CFTR protein is synthesized, traffics to its final destination, the plasma membrane, and is turned over. We will analyze distinctive advantages and drawbacks of these strategies in terms of their scientific and clinical dimensions, and we will propose a global strategy for CF research and development based on a reconciliatory approach. Moreover, we will discuss the utility of preclinical biomarkers that may guide the personalized, patient-specific implementation of CF therapies.
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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.