COVID-19 is widely epidemic in the world and poses a great threat to our life. Coagulopathy is one of the major characteristics in the
COVID-19 patients. A growing number of studies have found that the severe
COVID-19 patients have
thrombotic microangiopathy and
thromboembolism. Coagulopathy associated with increased risk of death in the patients. Unfortunately, the mechanism of coagulopathy is not clearly addressed. Understanding the pathophysiological mechanism of
COVID-19 thrombosis and improving the coagulopathy through efficient treatment may help to stop
disease progression, reduce mortality and sequelae. In severe
COVID-19 patients,
inflammation,
cytokine storm, and coagulation are closely related, which together cause blood congestion and
thrombosis. Many
cytokines activate blood cells, expressing activating factors or releasing activated microparticles, and then accelerating
thrombosis. However, the role of blood cells is not well understood in
COVID-19 patients. In addition,
cytokines stimulate endothelial cells, transforming them into a procoagulant phenotype. Therefore, determine their role and propose new strategies for the prevention and treatment of
thrombosis in severe
COVID-19 patients. We outline the major events of coagulopathies, discuss the role of blood and endothelial cells in
thrombosis, to formulate a new anticoagulation protocol.