ReviewExpert review of respiratory medicine
Interactions between calcium regulatory pathways and mechanosensitive channels in airways.
Review in Expert review of respiratory medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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
12 citing papers in PubMed, 13 citations in OpenAlex.
- Piezo1 mediates stretch-induced Wnt/β-catenin signaling and extracellular matrix remodeling in aging asthmatic airway smooth muscle.American journal of respiratory cell and molecular biology · 2026Article
- A 3D Astrocyte Microenvironment Model Enables Rapid CaAdvanced healthcare materials · 2026Article
- Integrating GPCR Regulation and Calcium Dynamics in Airway Smooth Muscle Function: A Comprehensive Review.Cells · 2026Review
- The importance of mechanical forces in chronic respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Mechanically induced dysregulation of calcium homeostasis: a molecular linchpin in asthmatic pathogenesis.European journal of medical research · 2025Review
- Mechanosensitive ion channels and inflammation: key links in cellular signal transduction.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Piezo proteins, mechano reception and behaviour in Hydra.Scientific reports · 2025Article
- Article
- Piezo channels modulate human lung fibroblast function.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Role of STIM1 in stretch-induced signaling in human airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Nicotinic receptors in airway disease.American journal of physiology. Lung cellular and molecular physiology · 2024Review
- 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
7 authors at 2 institutions in 2 countries.
Funding
Abstract
introductionAsthma is a chronic lung disease influenced by environmental and inflammatory triggers and involving complex signaling pathways across resident airway cells such as epithelium, airway smooth muscle, fibroblasts, and immune cells. While our understanding of asthma pathophysiology is continually progressing, there is a growing realization that cellular microdomains play critical roles in mediating signaling relevant to asthma in the context of contractility and remodeling. Mechanosensitive pathways are increasingly recognized as important to microdomain signaling, with Piezo and transient receptor protein (TRP) channels at the plasma membrane considered important for converting mechanical stimuli into cellular behavior. Given their ion channel properties, particularly Ca AREAS COVERED: Mechanosensitive TRP and Piezo channels regulate key Ca EXPERT OPINION: Physical and/or functional interactions between Ca
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.