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The alveolar surfactant film at the air–liquid interface is a thin, dynamic molecular layer that coats the inner surface of pulmonary alveoli. It is composed primarily of phospholipids (especially dipalmitoylphosphatidylcholine) and specific surfactant proteins (SP-A, SP-B, SP-C, SP-D), forming a structural continuum between an aqueous hypophase and inspired air[2][4]. Its central biological role is to dramatically reduce surface tension at the alveolar surface, thereby stabilizing alveoli against collapse during exhalation and facilitating efficient gas exchange[1][2][3][4]. This interface is not a homogeneous monolayer but a complex structure exhibiting dynamic phase transitions and structural heterogeneity depending on the local physical and physiological environment, with multilayered and monomolecular features observed under different states[1][2][3]. Surfactant dysfunction or deficiency is implicated in various respiratory diseases, particularly in premature infants and in conditions such as ARDS. This entity is a biophysical interface rather than a discrete molecular target like a receptor or enzyme, so does not fit the strict definition of a druggable therapeutic target, though it is the focus of important replacement therapies[3][4].
Surface-active agents replace or supplement natural surfactant to restore surface tension at the air–liquid interface and prevent alveolar collapse
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