New Insights into Airway Smooth Muscle: From Function to Dysfunction
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: 20 March 2025 | Viewed by 216
Special Issue Editor
Interests: respiratory medicine; allergy and pharmacology; β2-aderenergic agonists; muscarinic receptor antagonists; airway smooth muscle
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Airway smooth muscle cells play various physiological functions, such as contraction, proliferation, and migration. Functional phenotype changes in airway smooth muscle cells are probably associated with the fundamental pathophysiology of asthma, i.e., airflow limitation, airway hyperresponsiveness, β2-adrenergic desensitization, and airway remodeling. These phenotype changes are caused by the pathogenesis of asthma (type 2 and non-type 2 inflammation). Although, recently, various biological agents related to Th2 cytokines have been added to intensive controller medications using corticosteroids and long-acting bronchodilators for severe asthma, a dramatic advance in terms of the management of these patients has not been observed. Medical treatment focused on type 2 inflammation is often insufficient to maintain good long-term management for asthma. It is generally considered that asthma is complex and heterogenous. Therefore, it is necessary to promote research intracellular mechanisms underlying the effects of type 2 and non-type 2 inflammation on the physiological functions of airway smooth muscle cells in detail based on interactions with inflammatory cells (mast cells, eosinophils, and neutrophils) and epithelial cells. Recent studies have suggested novel therapeutic molecules for asthma that act on airway smooth muscle cells, such as glycolysis, ATP, IL-31, bitter taste receptor, myocardin, Nestin (a class VI intermediate filament protein), stromal-interacting molecule 1, and noncoding RNAs, etc. Oxidative stress and lysophospholipids may also be involved in the pathophysiology of asthma through effects on airway smooth muscle cells.
This Special Issue aims to provide a collection of studies focused on advancing therapy for asthma based on research into these phenotype changes related to pathophysiology in airway smooth muscle cells.
Prof. Dr. Hiroaki Kume
Guest Editor
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Keywords
- contraction
- proliferation
- migration
- airway hyperresponsiveness
- airway remodeling
- β2-adrenergic receptors
- muscarinic receptor
- Th2 inflammation
- non-Th2 inflammation
- oxidative stress
- lysophospholipids
- intracellular signal transduction processes
- Ca2+ signaling
- interactions with other cells (inflammatory cells and epithelium)
- asthma
- COPD
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