Neutrophil extracellular trap (NET) impact on deep vein thrombosis.
Deep vein thrombosis (DVT) is a major health problem that requires improved prophylaxis and treatment. Inflammatory conditions such as infection, cancer, and autoimmune diseases are risk factors for DVT. We and others have recently shown that extracellular DNA fibers produced in inflammation and known as neutrophil extracellular traps (NETs) contribute to experimental DVT. NETs stimulate thrombus formation and coagulation and are abundant in thrombi in animal models of DVT. It appears that, in addition to fibrin and von Willebrand factor, NETs represent a third thrombus scaffold. Here, we review how NETs stimulate thrombosis and discuss known and potential interactions of NETs with endothelium, platelets, red blood cells, and coagulation factors and how NETs could influence thrombolysis. We propose that drugs that inhibit NET formation or facilitate NET degradation may prevent or treat DVT.
Immune Disease Institute, Children’s Hospital Boston, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Tobias A
TA
Fuchs
Alexander
A
Brill
Denisa D
DD
Wagner
D000818:Animals; D001777:Blood Coagulation; D001792:Blood Platelets / Q000502:physiology; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000502:physiology; D004912:Erythrocytes / Q000502:physiology; D006801:Humans; D007113:Immunity, Innate; D061185:Mechanical Thrombolysis; D009504:Neutrophils / Q000502:physiology*; D013925:Thromboplastin / Q000502:physiology; D020246:Venous Thrombosis / Q000209:etiology*
D013925:Thromboplastin