Magnetically‐Induced Suppression of Oxidative Stress Prevents Venous Thrombosis

Venous thromboembolism (VTE) remains a leading cause of cardiovascular mortality. This study demonstrates that static magnetic fields (SMF) offer a novel non‐pharmacological intervention against VTE by mitigating endothelial oxidative stress. Mechanistically, SMF elevates intracellular Ca2+, boosts ATP production, and suppresses NOX4‐mediated ROS generation, ultimately reducing endothelial injury and thrombus formation, and improving survival in preclinical models. Abstract Venous thrombosis remains a major clinical challenge, with current therapeutic options limited by bleeding risks and procedural invasiveness. Here, it is demonstrated that static magnetic fields (SMFs) provide a non‐invasive and effective strategy for thrombosis prevention by mitigating oxidative damage to the vascular endothelium. In a murine model induced by FeCl3, exposure to SMFs significantly reduces thrombus formation, improves survival, and restores venous blood flow without affecting systemic coagulation or fibrinolytic pathways. Mechanistically, SMFs suppressed ROS accumulation and endothelial apoptosis in H2O2‐challenged vascular cells by elevating intracellular Ca2+ levels, which promotes ATP synthesis and suppress NOX4‐mediated oxidative stress. Furthermore, the protective effects of SMF against oxidative stress are largely diminished in the presence of either the calcium channel blocker or the specific NOX4 enzyme inhibitor. These findings reveal a Ca2+–ATP–NOX4 signaling axis as a key mediator of the vascular‐protective effects of SMFs, establishing a mechanistic rationale for their antithrombotic action. The consistent efficacy observed across varying SMF intensities underscores their translational potential as a next‐generation thromboprophylactic modality. Venous thromboembolism (VTE) remains a leading cause of cardiovascular mortality. This study demonstrates that static magnetic fields (SMF) offer a novel non-pharmacological intervention against VTE by mitigating endothelial oxidative stress. Mechanistically, SMF elevates intracellular Ca 2+, boosts ATP production, and suppresses NOX4-mediated ROS generation, ultimately reducing endothelial injury and thrombus formation, and improving survival in preclinical models. Abstract Venous thrombosis remains a major clinical challenge, with current therapeutic options limited by bleeding risks and procedural invasiveness. Here, it is demonstrated that static magnetic fields (SMFs) provide a non-invasive and effective strategy for thrombosis prevention by mitigating oxidative damage to the vascular endothelium. In a murine model induced by FeCl 3, exposure to SMFs significantly reduces thrombus formation, improves survival, and restores venous blood flow without affecting systemic coagulation or fibrinolytic pathways. Mechanistically, SMFs suppressed ROS accumulation and endothelial apoptosis in H 2 O 2 -challenged vascular cells by elevating intracellular Ca 2+ levels, which promotes ATP synthesis and suppress NOX4-mediated oxidative stress. Furthermore, the protective effects of SMF against oxidative stress are largely diminished in the presence of either the calcium channel blocker or the specific NOX4 enzyme inhibitor. These findings reveal a Ca 2+ –ATP–NOX4 signaling axis as a key mediator of the vascular-protective effects of SMFs, establishing a mechanistic rationale for their antithrombotic action. The consistent efficacy observed across varying SMF intensities underscores their translational potential as a next-generation thromboprophylactic modality. Advanced Science, EarlyView.