ArticleExpert opinion on therapeutic targets2011
CX3CR1 as a target for airways inflammation.
Article in Expert opinion on therapeutic targets, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Integrating multi-omics data of childhood asthma using a deep association model.Fundamental research · 2024Article
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- Circular RNA network plays a potential antiviral role in the early stage of JEV infection in mouse brain.Frontiers in microbiology · 2023Article
- CX3CL1 (fractalkine) and TNFα production by perfused human placental lobules under normoxic and hypoxic conditions in vitro: the importance of CX3CR1 signaling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Chorioamnionitis (ChA) modifies CX3CL1 (fractalkine) production by human amniotic epithelial cells (HAEC) under normoxic and hypoxic conditions.Journal of inflammation (London, England) · 2014Article
Corrections and comments
- Comment on
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is a key component of asthma. Membrane-bound chemokine CX3CL1 is markedly induced on endothelial cells by inflammatory cytokines, and CX3CL1 levels are elevated in the bronchoalveolar lavage (BAL) of subjects with asthma. Recently, CX3CR1 (the receptor for CX3CL1) has been proposed as a target for airway inflammation, and the paper proposing this was evaluated. The paper established a link between CX3CR1 and asthma, as reducing the availability of CX3CR1, or inhibiting the responses mediated by the CX3CR1, resulted in reduced asthma in a mouse model. This suggests that agents blocking the CX3CR1 may be useful in the treatment of asthma. However, there are reports suggesting that glucocorticoids may downregulate the CX3CL1-CX3CR1 pathway in inflammation. Thus, the next step is to establish whether inhibitors of the CX3CL1-CX3CR1 pathway have any additional, or different, effects to glucocorticoids, in the treatment of airway inflammatory disorders, in animal models. Subsequently, further consideration can be given to the development of CX3CR1 as a target for airway inflammation in humans.
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.