High altitude exposure is an important risk factor for thrombosis. The reporter learned from Kunming Institute of zoology, Chinese Academy of Sciences on September 5 that recently, the functional proteomics team of natural drugs led by researcher Lai Ren of the Institute has led to reveal the pathological mechanism of high altitude thrombosis, providing intervention strategies and new ideas for the research and development of new drugs against high altitude thrombosis. The internationally famous journal blood published relevant research results online. A large number of studies have shown that the incidence of venous and arterial thrombotic events is significantly increased at high altitude, including myocardial infarction, stroke, pulmonary embolism, cerebral venous thrombosis and portal vein thrombosis. The thrombotic tendency of people living at an altitude of 2000 meters is more than twice that of low-altitude people, while the risk of thrombotic disease of people living at an altitude of more than 3000 meters is 30 times that of low-altitude people. Although there have been some reports and hypotheses on the pathological mechanism of high altitude thrombosis, the research and hypothesis are still at a relatively shallow stage, and the key intermediate factors are still unknown. Therefore, it has become an urgent problem to study the pathogenesis of high altitude thrombosis and develop new antithrombotic strategies. Previously, Lai Ren's team had made a series of achievements in blood physiology, pathogenesis of thrombotic diseases and research and development of new antithrombotic drugs with low bleeding risk. Recently, in cooperation with researchers from the University of Toronto, they found that the concentration of transferrin, a key coagulation regulator, and the activities of thrombin and coagulation factor XIIa were significantly increased in the plasma of people living in high altitude areas for a long time and experimental mice traveling at high altitude for a short time. Subsequent animal and cell experiments confirmed that hypoxia and hypothermia, two key high altitude harmful factors, enhanced the expression of hypoxia inducible factor, which in turn promoted the expression of transferrin, further enhanced the activity of thrombin and this coagulation factor, and thus induced the tendency of plasma hypercoagulability. Studies have pointed out that high altitude transferrin is upregulated, which can increase iron ion transport and promote the maturation of bone marrow erythrocytes, thus increasing oxygen supply; Secondly, the upregulation of transferrin induces hypercoagulability and slows down blood circulation, thereby reducing heat loss and oxygen consumption, which may be an important physiological compensation strategy for organisms to cope with the two extreme environments of low oxygen and low temperature. Importantly, transferrin intervention, including transferrin antibody treatment, transferrin knockdown and designed polypeptides that inhibit the interaction between transferrin and coagulation factors, can effectively inhibit the occurrence of thrombotic events in high-altitude mouse models and improve the survival rate of mice. (outlook new era)