ArticleThorax2012
Aclidinium inhibits human lung fibroblast to myofibroblast transition.
Article in Thorax, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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, 65 citations in OpenAlex.
- Long-Acting Muscarinic Antagonists for the Treatment of Difficult-to-Treat and Severe Asthma: A Narrative Review Focusing on Inflammation from Bench to Bedside.Journal of inflammation research · 2026Review
- MUC4 is overexpressed in idiopathic pulmonary fibrosis and collaborates with transforming growth factor β inducing fibrotic responses.Mucosal immunology · 2021Article
- Neuroimmune Pathophysiology in Asthma.Frontiers in cell and developmental biology · 2021Review
- Pirfenidone anti-fibrotic effects are partially mediated by the inhibition of MUC1 bioactivation.Oncotarget · 2020Article
- Mechanical and Physical Regulation of Fibroblast-Myofibroblast Transition: From Cellular Mechanoresponse to Tissue Pathology.Frontiers in bioengineering and biotechnology · 2020Review
- Actin Alpha 2 (ACTA2) Downregulation Inhibits Neural Stem Cell Migration through Rho GTPase Activation.Stem cells international · 2020Article
- Fibroblast-to-myofibroblast transition in bronchial asthma.Cellular and molecular life sciences : CMLS · 2018Review
- The JAK2 pathway is activated in idiopathic pulmonary fibrosis.Respiratory research · 2018Article
- Combination of glycopyrronium and indacaterol inhibits carbachol-induced ERK5 signal in fibrotic processes.Respiratory research · 2017Article
- Non-neuronal cholinergic system contributes to corticosteroid resistance in chronic obstructive pulmonary disease patients.Respiratory research · 2016Article
- Haploinsufficiency of the folliculin gene leads to impaired functions of lung fibroblasts in patients with Birt-Hogg-Dubé syndrome.Physiological reports · 2016Article
- Combination therapy of tiotropium and ciclesonide attenuates airway inflammation and remodeling in a guinea pig model of chronic asthma.Respiratory research · 2016Article
- Review
- Restenosis after balloon valvuloplasty in a dog with pulmonary stenosis.The Journal of veterinary medical science · 2015Article
- Anticholinergics/antimuscarinic drugs in asthma.Current allergy and asthma reports · 2014Review
- Is there a rationale and role for long-acting anticholinergic bronchodilators in asthma?NPJ primary care respiratory medicine · 2014Article
- mAChRs activation induces epithelial-mesenchymal transition on lung epithelial cells.BMC pulmonary medicine · 2014Article
- Long-acting muscarinic receptor antagonists for the treatment of chronic airway diseases.Therapeutic advances in chronic disease · 2014Review
- Clinical potential of aclidinium bromide in chronic obstructive pulmonary disease.Therapeutics and clinical risk management · 2014Review
- 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
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFibroblast to myofibroblast transition is believed to contribute to airway remodelling in lung diseases such as asthma and chronic obstructive pulmonary disease. This study examines the role of aclidinium, a new long-acting muscarinic antagonist, on human fibroblast to myofibroblast transition.
methodsHuman bronchial fibroblasts were stimulated with carbachol (10(-8) to 10(-5) M) or transforming growth factor-β1 (TGF-β1; 2 ng/ml) in the presence or absence of aclidinium (10(-9) to 10(-7) M) or different drug modulators for 48 h. Characterisation of myofibroblasts was performed by analysis of collagen type I and α-smooth muscle actin (α-SMA) mRNA and protein expression as well as α-SMA microfilament immunofluorescence. ERK1/2 phosphorylation, RhoA-GTP and muscarinic receptors (M) 1, 2 and 3 protein expression were determined by western blot analysis and adenosine 3'-5' cyclic monophosphate levels were determined by ELISA. Proliferation and migration of fibroblasts were also assessed.
resultsCollagen type I and α-SMA mRNA and protein expression, as well as percentage α-SMA microfilament-positive cells, were upregulated in a similar way by carbachol and TGF-β1, and aclidinium reversed these effects. Carbachol-induced myofibroblast transition was mediated by an increase in ERK1/2 phosphorylation, RhoA-GTP activation and cyclic monophosphate downregulation as well as by the autocrine TGF-β1 release, which were effectively reduced by aclidinium. TGF-β1 activated the non-neuronal cholinergic system. Suppression of M1, M2 or M3 partially prevented carbachol- and TGF-β1-induced myofibroblast transition. Aclidinium dose-dependently reduced fibroblast proliferation and migration.
conclusionAclidinium inhibits human lung fibroblast to myofibrobast transition.
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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.