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The lung microvasculature is a hierarchical network of small blood vessels (arterioles, capillaries, venules) situated within the alveolar walls, primarily responsible for facilitating efficient gas exchange between air and blood. Beyond passive transport, this network plays active roles in immune surveillance, neutrophil margination, and rapid host defense against bloodstream pathogens, and supports alveolar cell maintenance and regeneration. The lung microvasculature is composed of diverse endothelial cell subtypes, including arterial, capillary (aerocyte and general), and venous endothelial cells, each expressing distinct molecular markers[2]. Microvascular dysfunction or remodeling is intimately involved in diseases such as COPD, pulmonary hypertension, and ARDS. While not a direct drug target itself, molecular components within the microvasculature (e.g., specific endothelial receptors, adhesion molecules) are key therapeutic targets and research foci[1][2][3][4][5]. Note: - The term "lung microvasculature" describes an anatomical-functional entity, not a specific molecule, gene, receptor, or protein, so it is not a conventional drug target. - Many drugs and therapies affect lung microvascular function through molecules expressed by its constituent endothelial or perivascular cells, but these components should be named specifically (e.g., "Vascular endothelial growth factor receptor 2", "Endothelin receptor type B", "PECAM1") for structured drug target workflows. - For structured target mapping, use the relevant cell type, receptor, or molecular target within the lung microvasculature.
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