ILLUMINATING ASTHMA’S COMPLEXITY: UNRAVELING THE MOLECULAR MECHANISM OF BETA-2 RECEPTOR AGONISTDRIVEN BRONCHIAL SMOOTH MUSCLE RELAXATION

Asthma is a common noncommunicable disease that causes airway inflammation, leading to airway hyperresponsiveness and airflow limitation due to reversible bronchoconstriction, increased mucus production, and complex airway inflammation. Despite this complexity, asthma treatments that include inhaling β2-agonists are widely used. Two types of bronchodilators are commonly used to treat bronchial asthma and chronic obstructive lung disease including β2-adrenoceptor agonists and theophylline. β2-receptor agonists activate phosphorylation mechanisms, as well as NO donors activate bronchial KCa2+ directly. These compounds stimulate cAMP- and cGMP-dependent protein kinases, which phosphorylate and activate bronchial KCa2+. Additionally, the role of exchange proteins directly activated by cAMP (Epac) in the relaxation of bronchial smooth muscle. Although β2-receptor agonists are known to relax bronchial smooth muscle, the exact molecular mechanism remains unclear. Therefore, the present study aims to elaborate on this mechanism and provide a more comprehensive understanding of β2-receptor agonist-mediated relaxation of bronchial smooth muscle in asthma. [Article No. 179] doi:10.21276/bpr.2023.13.2