ReviewCurrent opinion in pharmacology2010
beta-Adrenoceptor inverse agonists in asthma.
Review in Current opinion in pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.
- Pooled it
- Cardioselective beta-blocker use in patients with reversible airway disease.The Cochrane database of systematic reviews · 2001Pooled it
- Optical control of cell-surface and endomembrane-exclusive β-adrenergic receptor signaling.The Journal of biological chemistry · 2024Article
- Optical Control of Cell-Surface and Endomembrane-Exclusive β-Adrenergic Receptor Signaling.bioRxiv : the preprint server for biology · 2024Article
- The safety of cardioselective βERJ open research · 2021Review
- G Protein-Coupled Receptors in Asthma Therapy: Pharmacology and Drug Action.Pharmacological reviews · 2020Review
- Therapeutic Potential of Targeting ß-Arrestin.Frontiers in pharmacology · 2019Review
- Carvedilol inhibits EGF-mediated JB6 P+ colony formation through a mechanism independent of adrenoceptors.PloS one · 2019Article
- SUMOylation attenuates human β-arrestin 2 inhibition of IL-1R/TRAF6 signaling.The Journal of biological chemistry · 2015Article
- A-kinase anchoring proteins: cAMP compartmentalization in neurodegenerative and obstructive pulmonary diseases.British journal of pharmacology · 2014Review
- Role for β-arrestin in mediating paradoxical β2AR and PAR2 signaling in asthma.Current opinion in pharmacology · 2014Review
- β-Adrenoceptor modulation in chronic obstructive pulmonary disease: present and future perspectives.Drugs · 2013Review
- Inflammation signals airway smooth muscle cell proliferation in asthma pathogenesis.Multidisciplinary respiratory medicine · 2013Article
- β-Arrestins in the immune system.Progress in molecular biology and translational science · 2013Review
- Beta-blockers: friend or foe in asthma?International journal of general medicine · 2013Article
- Chronic treatment in vivo with β-adrenoceptor agonists induces dysfunction of airway β(2) -adrenoceptors and exacerbates lung inflammation in mice.British journal of pharmacology · 2012Article
- For the love of paradox: from neurobiology to pharmacology.Behavioural pharmacology · 2011Review
- Anti-asthma Drugs Formoterol and Budesonide (Symbicort) Induce Orofacial Clefts, Gastroschisis and Heart Septum Defects in anIn vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Beta(2)-adrenoceptor (beta(2)-AR) agonists are very effective bronchodilators and play a major role in every stage of asthma management. However, their chronic, regular use is associated with detrimental effects including an increase in asthma-related deaths. Conversely, recent data suggest that certain beta-blockers, specifically beta-adrenoceptor (beta-AR) inverse agonists, may be useful in the chronic treatment of asthma. Here we review the data for this observation and the signaling pathways that may be involved. The data suggest that beta(2)-AR signaling is required to produce maximal airway inflammation and hyperresponsiveness, and the signaling pathway responsible for these effects is likely the non-canonical beta-arrestin-2 pathway. Therefore, beta-AR inverse agonists may produce their beneficial chronic effects by inhibiting constitutive or ligand-induced activation of this pathway. Both lung parenchymal and hematopoietic cells appear to be involved in mediating the beneficial effects of beta-AR inverse agonists.
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.