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Background Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide, with smoking as major risk factor. Tobacco smoke increases the risk of thrombosis, resulting in dysregulation of tissue factor (TF)-mediated extrinsic coagulation that further impacts downstream intracellular signaling via protease activated receptors (PARs). Here, we investigated the impact of bronchial epithelial cell (BEC)-derived TF+-extracellular vesicles (EVs) on human lung endothelial cell (EC) activation as mediators of pulmo-vascular inflammation.
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Burhorst et al. (2024) studied this question.
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