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Airway sensory nerves are specialized afferent neurons—primarily originating from the vagal ganglia—that densely innervate the airway epithelium, smooth muscle, glands, and autonomic ganglia throughout the respiratory tract[1][2][3][4]. These nerves detect a broad spectrum of chemical and mechanical stimuli using an array of ion channels and receptors (e.g., TRPV1, P2X3), transmitting signals to the brainstem to coordinate protective airway reflexes including cough, bronchoconstriction, and modulation of breathing[1][2][3][6][7][9]. They can be classified as mechanoreceptors (primarily Aδ myelinated fibers responsive to touch/stretch) or chemoreceptors/nociceptors (primarily unmyelinated C-fibers responsive to chemical irritants and inflammation)[1][2][8][9]. Their activity is fundamental in both homeostasis and disease: neuronal plasticity, upregulation of ion channels, or increased neuropeptide release is linked to airway hyperreactivity, asthma, and chronic cough[1][2][3][7]. Therapeutic targeting of these nerves, particularly via P2X3 and TRPV1 channel antagonists, represents an area of active clinical development for chronic cough and other airway diseases[1][2][3][9]. Notes regarding target definition: - "Sensory nerves in airway" is not a singular molecular target but a heterogeneous population of sensory neurons defined by function, location, and molecular markers, encompassing multiple subtypes and receptors (e.g., TRPV1, P2X3, neuropeptide receptors)[1][2][3][4][6][7]. - For structured databases, this entry should be broken down into more specific molecular targets (such as "P2X3 receptor" or "Transient receptor potential vanilloid 1 [TRPV1]"), as "airway sensory nerve" itself is not a single defined target molecule but rather a functional/anatomical grouping[4][6][7][9]. Summary of incorrectness: - While the concept is valid and therapeutically relevant, the terminology is too broad for use as a unique canonical drug target—underlying molecular targets should be specified for structured data[4][6][7].
Inhibition of afferent nerve signaling, Antagonism of specific ion channels (P2X3, TRPV1), Blockade of neuropeptide release, Inhibition of neuronal excitability
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