ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
Adenosine and osteopontin contribute to the development of chronic obstructive pulmonary disease.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 51 citations in OpenAlex.
- Simvastatin up-regulates adenosine deaminase and suppresses osteopontin expression in COPD patients through an IL-13-dependent mechanism.Respiratory research · 2016Trial
- Loss of cPLA2α function attenuates inflammation and epithelial thickening in a mouse model ofCurrent research in microbial sciences · 2026Article
- Osteopontin promoted cardiac inflammation through increased interleukin-12 in acute myocarditis.Molecular biomedicine · 2025Article
- Early immune response toMicrobiology spectrum · 2025Article
- Secreted Phosphoprotein 1 in Lung Diseases.Metabolites · 2025Review
- Relationship between SPP1 (Osteopontin) and extracellular matrix dynamics: a comprehensive review.Frontiers in medicine · 2025Review
- Osteopontin: an essential regulatory protein in idiopathic pulmonary fibrosis.Journal of molecular histology · 2024Review
- Review
- Comparison of CRP, Procalcitonin, Neutrophil Counts, Eosinophil Counts, sTREM-1, and OPN between Pneumonic and Nonpneumonic Exacerbations in COPD Patients.Canadian respiratory journal · 2022Observational
- Adenosine and Inflammation: Here, There and Everywhere.International journal of molecular sciences · 2021Review
- Bioinformatics analysis of the potential biomarkers for acute respiratory distress syndrome.Bioscience reports · 2020Article
- Osteopontin Expression in Small Airway Epithelium in Copd is Dependent on Differentiation and Confined to Subsets of Cells.Scientific reports · 2019Article
- Adenosine and hyaluronan promote lung fibrosis and pulmonary hypertension in combined pulmonary fibrosis and emphysema.Disease models & mechanisms · 2019Article
- Purinergic Signaling in Pulmonary Inflammation.Frontiers in immunology · 2019Review
- Chemokine (C-C Motif) Receptor-Like 2 is not essential for lung injury, lung inflammation, or airway hyperresponsiveness induced by acute exposure to ozone.Physiological reports · 2017Article
- Mediation of the single-walled carbon nanotubes induced pulmonary fibrogenic response by osteopontin and TGF-β1.Experimental lung research · 2017Article
- Loss of CD73 prevents accumulation of alternatively activated macrophages and the formation of prefibrotic macrophage clusters in irradiated lungs.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Adenosine and adenosine receptors in the pathogenesis and treatment of rheumatic diseases.Nature reviews. Rheumatology · 2017Review
- Extracellular Adenosine Production by ecto-5'-Nucleotidase (CD73) Enhances Radiation-Induced Lung Fibrosis.Cancer research · 2016Article
- Combined inhibition of TGFβ and PDGF signaling attenuates radiation-induced pulmonary fibrosis.Oncoimmunology · 2016Article
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
Chronic obstructive pulmonary disease (COPD) is a major health concern. Adenosine, a signaling molecule generated in response to cell stress, contributes to the pathogenesis of COPD. An established model of adenosine-mediated lung injury is the adenosine deaminase-deficient (Ada(-/-)) mouse. Osteopontin (OPN) is a chemokine that is produced following injury and is implicated in a variety of human pathologies, but its expression and role in the pathogenesis of COPD have not been examined. To investigate the role of OPN in a model of COPD, Ada(-/-) double-knockout mice were generated, and inflammation and air-space enlargement endpoints were examined. Results demonstrate that Ada(-/-) mice exhibit OPN-dependent neutrophilia, alveolar air-space enlargement, and increases in mediators of air-space enlargement. Furthermore, we demonstrate that patients with COPD have increased OPN expression within distal airways in association with clinical airway obstruction. These results suggest that OPN represents a novel biomarker and therapeutic target for patients with COPD.
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.