Alveolar–capillary barrier

The **alveolar–capillary barrier** (also called the blood–air barrier or alveolar–capillary membrane) is a structural and functional interface in the lung, not a single molecule or classic druggable target. It comprises the alveolar epithelial cells (mainly type I and type II pneumocytes), the basement membrane, and the adjacent capillary endothelial cells[1][2][5][6][9]. This barrier is essential for rapid and efficient gas exchange (oxygen and carbon dioxide) between alveolar airspaces and blood, permits the lung to remain dry by preventing fluid leakage, and prevents the passage of large solutes or pathogens from the bloodstream into the airspaces. It maintains homeostasis via the integrity of cell layers and surfactant production, and its derangement can result in pulmonary edema, acute respiratory distress syndrome, and respiratory failure[1][2][4][9]. Because this term refers to a multi-cellular tissue architecture and not a receptor, enzyme, transporter, or other molecular target, it is not considered a conventional therapeutic target, though its integrity and function are central in lung disease pathophysiology. Key clarification: - "Lung airspaces and alveolar–capillary barrier" describes a histological structure rather than a druggable molecular target (such as a receptor, ion channel, enzyme, etc.), so **is_target: false** and **is_incorrect: true** (not a target under standard pharmacological conventions)[1][2][5]. - Component molecules (such as surfactant proteins or specific cell surface markers) may be targeted, but the barrier itself is not a discrete molecular entity.

Other names

Blood–air barrierAir–blood barrierAlveolar–capillary membraneBlood–gas barrier