ArticleAmerican journal of respiratory cell and molecular biology2025
TMEM16A Antagonism: Therapeutic Potential with Desensitization of β-Agonist Responsiveness in Asthma.
Article in American journal of respiratory cell and molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Helper T cells and chemokines in elderly asthma - Mechanisms of airway inflammation and remodeling: A review.Biomolecules & biomedicine · 2026Review
- Research and optimization of screening strategy for calcium-activated chloride channel modulators guided by electrophysiological characteristics.Scientific reports · 2026Article
- Implicates of PIP5K1α in asthma-related biological processes: insights into mechanisms and therapeutic potential.Journal of translational medicine · 2025Review
- Channeling Relaxation through Multiple Means: TMEM16A Antagonism for Asthma.American journal of respiratory cell and molecular biology · 2025Article
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7 authors.
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Abstract
The efficacy of β-agonists in asthma is severely limited by β-adrenoceptor desensitization, which results in poorly managed symptoms and refractory bronchoconstriction. Thus, there is a need to identify novel therapeutic pathways and to clarify the relationship between novel therapeutics and functional β-adrenoceptor responsiveness. We have previously demonstrated that acute antagonism of the calcium-activated chloride channel, transmembrane member 16A (TMEM16A), relaxes airway smooth muscle (ASM). We sought to determine the efficacy and role of TMEM16A antagonism in the context of desensitization β-adrenoceptor responsiveness. For these studies, we exposed murine tracheal rings on wire myography and precision-cut lung slices to contractile mediators in the presence or absence of TMEM16A antagonists and β-agonists with or without prior β-adrenoceptor desensitization. Contractile studies were also performed with human tracheal and bronchial ASM. Finally, the ability of TMEM16A antagonism to prevent desensitization of β
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