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<p>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.</p>

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Prevention of acute thrombosis with vascular endothelium antioxidative nanoscavenger

  • 期刊论文

  • 发表日期：

    2025年10月31日

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  • Yixin Zhong,
  • Qiankun Ni,
  • Liandi Huang,
  • Guangchao Qing,
  • Fuxue Zhang,
  • Ningqiang Gong,
  • Hongyun Wu,
  • Yukun Liao,
  • Huiting Jiang,
  • Zaiqian Tu,
  • Zhifei Wang,
  • Luksika Jiramonai,
  • Haidong Zhu,
  • Gao-Jun Teng,
  • Xing-Jie Liang

摘要

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.