ReviewDrugs2014
Asthma therapy and its effect on airway remodelling.
Review in Drugs, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Vitamin D supplementation in pregnant or breastfeeding women or young children for preventing asthma.The Cochrane database of systematic reviews · 2025Pooled it
- Lycopene inhibits airway remodeling in allergic asthma models by suppressing the epithelial-mesenchymal transformation in airway epithelial cells.European journal of nutrition · 2026Article
- ITGA5 as a Dual Regulator of Epithelial-Mesenchymal Transition and Epithelial Cell Anoikis Resistance: Functional Validation and Drug Prediction.Cell proliferation · 2026Article
- EV-associated non-coding RNAs in paediatric asthma airway remodelling: current mechanistic evidence and therapeutic perspectives.Frontiers in pharmacology · 2026Review
- Oxidative stress in asthma pathogenesis: mechanistic insights and implications for airway smooth muscle dysfunction.Cell and tissue research · 2025Review
- New insights into mesenchymal stem cells in inflammatory subtypes of asthma.Frontiers in immunology · 2025Review
- Nicotine affects mitochondrial structure and function in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Current and future developments in the pharmacology of asthma and COPD: ERS seminar, Naples 2022.Breathe (Sheffield, England) · 2023Review
- Airway remodeling heterogeneity in asthma and its relationship to disease outcomes.Frontiers in physiology · 2023Review
- Medicine Targeting Epithelial-Mesenchymal Transition to Treat Airway Remodeling and Pulmonary Fibrosis Progression.Canadian respiratory journal · 2023Review
- A review of the pathophysiology and the role of ion channels on bronchial asthma.Frontiers in pharmacology · 2023Review
- Airway smooth muscle in contractility and remodeling of asthma: potential drug target mechanisms.Expert opinion on therapeutic targets · 2023Article
- Asthma and Post-Asthmatic Fibrosis: A Search for New Promising Molecular Markers of Transition from Acute Inflammation to Pulmonary Fibrosis.Biomedicines · 2022Article
- Pan-Phosphodiesterase Inhibitors Attenuate TGF-β-Induced Pro-Fibrotic Phenotype in Alveolar Epithelial Type II Cells by Downregulating Smad-2 Phosphorylation.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Asthma with Fixed Airflow Obstruction: From Fixed to Personalized Approach.Journal of personalized medicine · 2022Review
- Nicotinic α7 acetylcholine receptor (α7nAChR) in human airway smooth muscle.Archives of biochemistry and biophysics · 2021Article
- Sinomenine Relieves Airway Remodeling By Inhibiting Epithelial-Mesenchymal Transition Through Downregulating TGF-β1 and Smad3 ExpressionFrontiers in immunology · 2021Article
- Progranulin Protects Against Airway Remodeling Through the Modulation of Autophagy via HMGB1 Suppression in House Dust Mite-Induced Chronic Asthma.Journal of inflammation research · 2021Article
- Metabolic Adaptation of Airway Smooth Muscle Cells to an SPHK2 Substrate Precedes Cytostasis.American journal of respiratory cell and molecular biology · 2020Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Asthma remains a major health problem with significant morbidity, mortality and economic costs. In asthma, airway remodelling, which refers to all the microscopic structural changes seen in the airway tissue, has been recognised for many decades and remains one of the defining characteristics of the disease; however, it is still poorly understood. The detrimental pathophysiological consequences of some features of remodelling, like increased airway smooth muscle mass and subepithelial fibrosis, are well documented. However, whether targeting these by therapy would be beneficial is unknown. Although the prevailing thinking is that remodelling is an abnormal response to persistent airway inflammation, recent evidence, especially from studies of remodelling in asthmatic children, suggests that the two processes occur in parallel. The effects of asthma therapy on airway remodelling have not been studied extensively due to the challenges of obtaining airway tissue in the context of clinical trials. Corticosteroids remain the cornerstone of asthma therapy, and their effects on remodelling have been better studied than other drugs. Bronchial thermoplasty is the only asthma therapy to primarily target remodelling, although how it results in the apparent clinical benefits seen is not exactly clear. In this article we discuss the mechanisms of airway remodelling in asthma and review the effects of conventional and novel asthma therapies on the process.
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.