ArticleThe open respiratory medicine journal2010
Antiproteases as therapeutics to target inflammation in cystic fibrosis.
Article in The open respiratory medicine journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
What it found
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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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- The emerging role of immunothrombosis in paediatric conditions.Pediatric research · 2019Pooled it
- Neutrophil serine proteases in cystic fibrosis: role in disease pathogenesis and rationale as a therapeutic target.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Protease inhibitors elicit anti-inflammatory effects in CF mice with Pseudomonas aeruginosa acute lung infection.Clinical and experimental immunology · 2021Article
- Alginate/Chitosan Particle-Based Drug Delivery Systems for Pulmonary Applications.Pharmaceutics · 2019Article
- Role of IRE1α/XBP-1 in Cystic Fibrosis Airway Inflammation.International journal of molecular sciences · 2017Review
- Protease Inhibitors in Tick Saliva: The Role of Serpins and Cystatins in Tick-host-Pathogen Interaction.Frontiers in cellular and infection microbiology · 2017Review
- NETs and CF Lung Disease: Current Status and Future Prospects.Antibiotics (Basel, Switzerland) · 2015Review
- Regulation of TGF-β1-driven differentiation of human lung fibroblasts: emerging roles of cathepsin B and cystatin C.The Journal of biological chemistry · 2014Article
- Inter-α-inhibitor blocks epithelial sodium channel activation and decreases nasal potential differences in ΔF508 mice.American journal of respiratory cell and molecular biology · 2014Article
- 2-O, 3-O-desulfated heparin inhibits neutrophil elastase-induced HMGB-1 secretion and airway inflammation.American journal of respiratory cell and molecular biology · 2014Article
- Cystic fibrosis: a mucosal immunodeficiency syndrome.Nature medicine · 2012Review
- Neutrophil elastase inhibitors.Expert opinion on therapeutic patents · 2011Review
- Human cysteine cathepsins are not reliable markers of infection by Pseudomonas aeruginosa in cystic fibrosis.PloS one · 2011Article
- Neutrophil elastase, proteinase 3, and cathepsin G as therapeutic targets in human diseases.Pharmacological reviews · 2010Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic Fibrosis (CF) is the most common fatal inherited disease of Caucasians, affecting about 1 in 3000 births. Patients with CF have a recessive mutation in the gene encoding the CF transmembrane conductance regulator (CFTR). CFTR is expressed in the epithelium of many organs throughout the exocrine system, however, inflammation and damage of the airways as a result of persistent progressive endobronchial infection is a central feature of CF. The inflammatory response to infection brings about a sustained recruitment of neutrophils to the site of infection. These neutrophils release various pro-inflammatory compounds including proteases, which when expressed at aberrant levels can overcome the endogenous antiprotease defence mechanisms of the lung. Unregulated, these proteases can exacerbate inflammation and result in the degradation of structural proteins and tissue damage leading to bronchiectasis and loss of respiratory function. Other host-derived and bacterial proteases may also contribute to the inflammation and lung destruction observed in the CF lung. Antiprotease strategies to dampen the excessive inflammatory response and concomitant damage to the airways remains an attractive therapeutic option for CF patients.
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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.