ArticleProceedings of the National Academy of Sciences of the United States of America2009
Beta2-adrenoceptor signaling is required for the development of an asthma phenotype in a murine model.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00670267 (An Open-Label, Dose-Escalating, Study to Evaluate the Safety, Efficacy and Tolerability of Oral Nadolol for the Treatment of Adults With Mild Asthma), which is not on this map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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.
An Open-Label, Dose-Escalating, Study to Evaluate the Safety, Efficacy and Tolerability of Oral Nadolol for the Treatment of Adults With Mild Asthma
Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.
- Pooled it
- Effects of hydrocortisone on acute β-adrenoceptor blocker and histamine induced bronchoconstriction.British journal of clinical pharmacology · 2012Trial
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- Qualitative beta-2-adrenoceptor signaling in the regulation of human airway epithelia mucin and cytokine production.Respiratory research · 2026Article
- Biased Orthosteric Agonism and Allosteric Modulation: Emerging Strategies for Developing New Class of β-Agonists for Obstructive Airway Diseases.American journal of respiratory cell and molecular biology · 2025Review
- Airway sympathectomy attenuates inflammation, transcriptional ratios of Muc5ac and Muc5b, and airway mechanic deficits in mice delivered intranasal IL-13.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Inhibition of TRPA1, Endoplasmic Reticulum Stress, Human Airway Epithelial Cell Damage, and EctopicPharmaceuticals (Basel, Switzerland) · 2023Article
- Fusion of the βFASEB bioAdvances · 2022Article
- S-nitrosylation is required for βMolecular cell · 2022Article
- Oral antibiotics relieve allergic asthma in post-weaning miceFrontiers in immunology · 2022Article
- Cooperativity between β-agonists and c-Abl inhibitors in regulating airway smooth muscle relaxation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Can GPCRs Be Targeted to Control Inflammation in Asthma?Advances in experimental medicine and biology · 2021Article
- Phosphodiesterase isoforms and cAMP compartments in the development of new therapies for obstructive pulmonary diseases.Current opinion in pharmacology · 2020Review
- The dopamine DRespiratory research · 2018Article
- Article
- βProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Effects of β-blockers on house dust mite-driven murine models pre- and post-development of an asthma phenotype.Pulmonary pharmacology & therapeutics · 2017Article
- Proinflammatory Cytokines Mediate GPCR Dysfunction.Journal of cardiovascular pharmacology · 2017Review
- βScientific reports · 2017Article
- Biphasic effects of propranolol on tumour growth in B16F10 melanoma-bearing mice.British journal of pharmacology · 2017Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic regular use of beta(2)-adrenoceptor (beta(2)-AR) agonists in asthma is associated with a loss of disease control and increased risk of death. Conversely, we have found that administration of beta(2)-AR inverse agonists results in attenuation of the asthma phenotype in an allergen-driven murine model. Besides antagonizing agonist-induced signaling and reducing signaling by empty receptors, beta-AR inverse agonists can also activate signaling by novel pathways. To determine the mechanism of the beta-AR inverse agonists, we compared the asthma phenotype in beta(2)-AR-null and wild-type mice. Antigen challenge of beta(2)-AR-null mice produced results similar to what was observed with chronic beta(2)-AR inverse agonist treatment, namely, reductions in mucous metaplasia, airway hyperresponsiveness (AHR), and inflammatory cells in the lungs. These results indicate that the effects of beta(2)-AR inverse agonists are caused by inhibition of beta(2)-AR signaling rather than by the induction of novel signaling pathways. Chronic administration of alprenolol, a beta-blocker without inverse agonist properties, did not attenuate the asthma phenotype, suggesting that it is signaling by empty receptors, rather than agonist-induced beta(2)-AR signaling, that supports the asthma phenotype. In conclusion, our results demonstrate that, in a murine model of asthma, beta(2)-AR signaling is required for the full development of three cardinal features of asthma: mucous metaplasia, AHR, and the presence of inflammatory cells in the lungs.
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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.