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**Bronchoconstriction** refers to the narrowing of the airways in the lungs due to contraction of smooth muscle surrounding the bronchi and bronchioles. This physiological response restricts airflow and can cause symptoms such as wheezing, coughing, chest tightness, and shortness of breath. It commonly occurs in conditions like asthma and COPD but can also be triggered by allergens, cold air, exercise (exercise-induced bronchoconstriction), environmental pollutants, smoke, chemicals, respiratory infections, stress, or anaphylaxis[1][3][5]. The underlying mechanism often involves activation of parasympathetic nerves releasing acetylcholine onto muscarinic M3 receptors on airway smooth muscle cells. This leads to increased intracellular calcium via G protein-coupled signaling pathways and results in muscle contraction[3]. Bronchoconstriction is not itself a druggable molecular target like a receptor or enzyme; rather it describes a pathophysiological state resulting from multiple upstream triggers. **Note:** "Bronchoconstriction" is not a molecule/receptor/protein/enzyme/transporter—it is a physiological process describing airway narrowing due to smooth muscle contraction. Therefore it does **not** fit standard definitions for therapeutic targets used in drug discovery databases. Drugs may act on specific targets involved in this process—such as muscarinic acetylcholine receptors or beta2-adrenoceptors—but "bronchoconstriction" itself cannot be considered such a target[1][3][5].
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