ArticleAmerican journal of respiratory cell and molecular biology2008
A3 adenosine receptor signaling influences pulmonary inflammation and fibrosis.
Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 51 citations in OpenAlex.
- Network toxicology reveals key genes of amiodarone induced pulmonary fibrosis: based on machine learning and SHAP analysis.Frontiers in pharmacology · 2026Article
- Does Adenosine Triphosphate via Purinergic Receptor Signalling Fuel Pulmonary Fibrosis?Journal of innate immunity · 2025Review
- Adenosine AInternational journal of molecular sciences · 2022Article
- A novel definition and treatment of hyperinflammation in COVID-19 based on purinergic signalling.Purinergic signalling · 2022Review
- Adenosine and Inflammation: Here, There and Everywhere.International journal of molecular sciences · 2021Review
- Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis.Cellular and molecular life sciences : CMLS · 2021Review
- LJ-2698, an Adenosine A3 Receptor Antagonist, Alleviates Elastase-Induced Pulmonary Emphysema in Mice.Biomolecules & therapeutics · 2020Article
- Review
- Ability of CP-532,903 to protect mouse hearts from ischemia/reperfusion injury is dependent on expression of ABiochemical pharmacology · 2019Article
- Targeting the Immunomodulatory CD73/Adenosine System to Improve the Therapeutic Gain of Radiotherapy.Frontiers in immunology · 2019Review
- AMedicinal research reviews · 2018Review
- Purinergic signalling links mechanical breath profile and alveolar mechanics with the pro-inflammatory innate immune response causing ventilation-induced lung injury.Purinergic signalling · 2017Review
- Extracellular Adenosine Production by ecto-5'-Nucleotidase (CD73) Enhances Radiation-Induced Lung Fibrosis.Cancer research · 2016Article
- Rational design of sulfonated A3 adenosine receptor-selective nucleosides as pharmacological tools to study chronic neuropathic pain.Journal of medicinal chemistry · 2013Article
- Sustained adenosine exposure causes lung endothelial barrier dysfunction via nucleoside transporter-mediated signaling.American journal of respiratory cell and molecular biology · 2012Article
- Truncated Nucleosides as A(3) Adenosine Receptor Ligands: Combined 2-Arylethynyl and Bicyclohexane Substitutions.ACS medicinal chemistry letters · 2012Article
- Investigational A₃ adenosine receptor targeting agents.Expert opinion on investigational drugs · 2011Review
- Distinct roles for the A2B adenosine receptor in acute and chronic stages of bleomycin-induced lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Animal models of airway diseases.Sub-cellular biochemistry · 2011Review
- Targeting of adenosine receptors in ischemia-reperfusion injury.Expert opinion on therapeutic targets · 2011Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Adenosine is a signaling molecule produced during conditions that cause cellular stress or damage. This signaling pathway is implicated in the regulation of pulmonary disorders through the selective engagement of adenosine receptors. The goal of this study was to examine the involvement of the A(3) adenosine receptor (A(3)R) in a bleomycin model of pulmonary inflammation and fibrosis. Results demonstrated that A(3)R-deficient mice exhibit enhanced pulmonary inflammation that included an increase in eosinophils. Accordingly, there was a selective up-regulation of eosinophil-related chemokines and cytokines in the lungs of A(3)R-deficient mice exposed to bleomycin. This increase in eosinophil numbers was accompanied by a decrease in the amount of extracellular eosinophil peroxidase activity in lavage fluid from A(3)R-deficient mice exposed to bleomycin, an observation suggesting that the A(3)R is necessary for eosinophil degranulation in this model. Despite an increase in inflammatory metrics associated with A(3)R-deficient mice treated with bleomycin, there was little difference in the degree of pulmonary fibrosis. Examination of fibrotic mediators demonstrated enhanced transforming growth factor (TGF)-beta1 expression, but not a concomitant increase in TGF-beta1 activity. This was associated with the loss of expression of matrix metalloprotease 9, an activator of TGF-beta1, in alveolar macrophages and airway mast cells in the lungs of A(3)R-deficient mice. Together, these results suggest that the A(3)R serves antiinflammatory functions in the bleomycin model, and is also involved in regulating the production of mediators that can impact fibrosis.
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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.