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Updated: May 13, 2025

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
Vanadia Nanozymes Inhibit Platelet Aggregation, Modulate Signaling Pathways and Prevent Pulmonary Embolism in Mice
G R Sherin1, Bidare N SharathBabu1, Kurnegala Manikanta2
1Department of Inorganic and Physical Chemistry, Indian Institute of Science, Bangalore, 560012, India.
Abstract:
Thrombosis is a pathological condition which represents the formation of clots inside blood vessels, blocking the flow of blood through the circulatory system. A high occurrence of thrombotic events, particularly deep vein thrombosis and pulmonary embolism, has been observed in COVID-19 patients. Platelets (thrombocytes), the small cell fragments in the blood, play crucial roles in vascular haemostasis and thrombosis. The activation and subsequent aggregation of platelets lead to the formation of thrombus, a key process in the development of cardiovascular diseases. Therefore, inhibitors of platelet aggregation are important for the prevention and treatment of many thrombotic disorders. As the selenoenzyme glutathione peroxidase (GPx) is known to prevent platelet-dependent thrombosis, we have studied a series of antioxidant nanozymes for their ability to inhibit platelet activation/aggregation. Herein, we show that V2O5 nanozymes with specific and morphology-dependent GPx activity effectively inhibit the aggregation of human platelets and prevent pulmonary thromboembolism in mice. Crucially, the nanozymes do not lead to the unwanted side effect of bleeding, which is important in the development of more effective and safe antithrombotic agents.
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