Prevention of acute thrombosis with vascular endothelium antioxidative nanoscavenger
Antiplatelet drugs have represented a milestone in treating patients at high risk of thrombosis. However, their clinical use remains limited by bleeding-associated risk and limited efficacy. Excessive reactive oxygen species (ROS) produced by damaged vascular endothelial cells, have been shown to stimulate thrombosis. Here, we propose that a ROS-chemotactic nanoscavenger (MDCP), formed by crosslinking melanin and catalase, prevents acute thrombosis by protecting vascular endothelial cells from oxidative stress. We demonstrate that treatment with MDCP inhibits ROS-induced apoptosis of endothelial cells, thereby maintaining endothelial integrity and preventing collagen exposure, which consequently prevents platelet activation and thrombosis. By avoiding direct interference with platelet function, this modulation of vascular redox homeostasis via MDCP provides a promising alternative antithrombotic strategy that addresses the bleeding risk of current clinical antithrombotic drugs. Overall design: Transcriptomic profiles of rat abdominal aortas comparing FeCl3-induced thrombosis to saline control. The dataset includes 4 biologically independent replicates per condition.