Abstract
Neutrophils play a vital role in the formation of arterial, venous and cancer-related thrombosis. Recent studies have shown that in a process known as NETosis, neutrophils release proteins and enzymes complexed to DNA fibers, collectively called neutrophil extracellular traps (NETs). Although NETs were originally described as a way for the host to capture and kill bacteria, current knowledge indicates that NETs also play an important role in thrombosis. According to recent studies, the destruction of vascular microenvironmental homeostasis and excessive NET formation lead to pathological thrombosis. In vitro experiments have found that NETs provide skeletal support for platelets, red blood cells and procoagulant molecules to promote thrombosis. The protein components contained in NETs activate the endogenous coagulation pathway to promote thrombosis. Therefore, NETs play an important role in the formation of arterial thrombosis, venous thrombosis and cancer-related thrombosis. This review will systematically summarize and explain the study of NETs in thrombosis in animal models and in vivo experiments to provide new targets for thrombosis prevention and treatment.
Highlights
The role of neutrophil extracellular traps (NETs) in inflammation and thrombosis has been controversial for decades [1, 2]
Many studies have confirmed an important role for NETs in the processes of atherosclerosis, coronary artery disease (CAD) and ischemic stroke [14,15,16]
As a scaffold for cells and various coagulation factors, NETs exist in plaques and thrombi and induce oxidative stress, induce the activation of endothelial cells, antigen-presenting cells and platelets, increase the expression of coagulation factors, and lead to proinflammatory reactions (Figure 2A). These structures play a role in the pathogenesis of atherosclerotic plaque formation and thrombosis [3, 4, 27]
Summary
The role of neutrophil extracellular traps (NETs) in inflammation and thrombosis has been controversial for decades [1, 2]. Many studies have confirmed an important role for NETs in the processes of atherosclerosis, coronary artery disease (CAD) and ischemic stroke [14,15,16]. Most of these studies are based on in vitro and animal experiments (Table 1). As a scaffold for cells and various coagulation factors, NETs exist in plaques and thrombi and induce oxidative stress, induce the activation of endothelial cells, antigen-presenting cells and platelets, increase the expression of coagulation factors, and lead to proinflammatory reactions (Figure 2A) These structures play a role in the pathogenesis of atherosclerotic plaque formation and thrombosis [3, 4, 27]. The specific deletion of peptidyl arginine deiminase-4 (PAD4) reduces the formation of NETs and significantly alleviates atherosclerosis, complications, and inflammation caused by macrophages [34, 35]
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