ReviewCurrent drug targets2016
Dysregulated Chemokine Signaling in Cystic Fibrosis Lung Disease: A Potential Therapeutic Target.
Review in Current drug targets, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 29 citations in OpenAlex.
- Trial
- Trial
- Peripheral leukocyte transcriptomic changes in preweaned Holstein heifer calves with varying stages of Bovine Respiratory Disease.PloS one · 2026Article
- TGF-β induces excessive pulmonary IL-6 secretion in cystic fibrosis via PI3K.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Elexacaftor/tezacaftor/ivacaftor (ETI) therapy modifies the expression of interferon beta and inflammatory genes in the airways of adult patients with cystic fibrosis: a pilot study.Molecular and cellular biochemistry · 2025Article
- Targeting the MEK1/2 pathway to combatmBio · 2025Article
- Elevated Immunoglobulin G as a Predictor of Progression to Severe Lung Disease in Cystic Fibrosis: A Longitudinal Cohort Study.Journal of clinical medicine · 2025Article
- miRNA-target gene network analysis in siblings with cystic fibrosis and phenotypic variability.Turkish journal of medical sciences · 2025Article
- Neutrophil-Derived Proteases in Lung Inflammation: Old Players and New Prospects.International journal of molecular sciences · 2024Review
- Review
- Genome-wide DNA methylation and transcriptome expression profiles of peripheral blood mononuclear cells in patients with systemic sclerosis with interstitial lung disease.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
- Impact ofInternational journal of molecular sciences · 2022Review
- Immunometabolism in biofilm infection: lessons from cancer.Molecular medicine (Cambridge, Mass.) · 2022Review
- MSCs interaction with the host lung microenvironment: An overlooked aspect?Frontiers in immunology · 2022Review
- Insulin-Like Growth Factor Binding Protein (IGFBP-6) as a Novel Regulator of Inflammatory Response in Cystic Fibrosis Airway Cells.Frontiers in molecular biosciences · 2022Article
- Two Siblings Homozygous for F508del-CFTR Have Varied Disease Phenotypes and Protein Biomarkers.International journal of molecular sciences · 2021Article
- The Multifaceted Roles of MicroRNAs in Cystic Fibrosis.Diagnostics (Basel, Switzerland) · 2020Review
- UnderstandingCells · 2020Review
- Factoring in the Complexity of the Cystic Fibrosis Lung to UnderstandPathogens (Basel, Switzerland) · 2020Review
- Salivary Cytokines and Airways Disease Severity in Patients with Cystic Fibrosis.Diagnostics (Basel, Switzerland) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
CF lung disease is characterized by a chronic and non-resolving activation of the innate immune system with excessive release of chemokines/cytokines including IL-8 and persistent infiltration of immune cells, mainly neutrophils, into the airways. Chronic infection and impaired immune response eventually lead to pulmonary damage characterized by bronchiectasis, emphysema, and lung fibrosis. As a complete knowledge of the pathways responsible for the exaggerated inflammatory response in CF lung disease is lacking, understanding these pathways could reveal new therapeutic targets, and lead to novel treatments. Therefore, there is a strong rationale for the identification of mechanisms and pathways underlying the exaggerated inflammatory response in CF lung disease. This article reviews the role of inflammation in the pathogenesis of CF lung disease, with a focus on the dysregulated signaling involved in the overexpression of chemokine IL-8 and excessive recruitment of neutrophils in CF airways. The findings suggest that targeting the exaggerated IL-8/IL-8 receptor (mainly CXCR2) signaling pathway in immune cells (especially neutrophils) may represent a potential therapeutic strategy for CF lung disease.
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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.