The Role of Hypoxia in Vascular Endothelial Dysfunction and Venous Thromboembolism.

This review explores the role of hypoxia in vascular endothelial dysfunction and its contribution to venous thromboembolism (VTE), including deep vein thrombosis and pulmonary embolism. It highlights the unique microenvironment of venous valvular sinuses, where stasis and hypoxia promote endothelial activation, inflammation, and coagulation. Key mechanisms, such as hypoxia-inducible factors, reactive oxygen species, and calcium signaling, are discussed in the context of thrombus formation. The review also examines advanced methodologies, including Vein-Chip and vascular organoids, for studying hypoxia-driven processes, and emphasizes the need for patient-specific models to improve understanding and therapeutic strategies for VTE.