Inflammation, innate immunity and blood coagulation.
Inflammation drives arterial, venous and microvascular thrombosis. Chronic inflammation contributes to arterial thrombotic complications, whereas acute inflammation drives venous thrombosis and microvascular thrombosis. Mechanistically, inflammation modulates thrombotic responses by upregulating procoagulants, downregulating anticoagulants and suppressing fibrinolysis. The inflammatory response can also result in cell apoptosis or necrosis. Products released from the dead cells, particularly histones, propagate further inflammation, tissue death and organ failure. Inhibition of histone mediated cytotoxicity appears to be a new mechanism for protecting against this deadly cascade.
Xu
J
J
Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.
Lupu
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F
Esmon
C T
CT
D000925:Anticoagulants / Q000494:pharmacology; D001777:Blood Coagulation / Q000276:immunology / Q000502:physiology*; D016923:Cell Death; D005342:Fibrinolysis / Q000502:physiology; D006657:Histones / Q000037:antagonists & inhibitors; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000150:complications / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D013927:Thrombosis / Q000209:etiology / Q000503:physiopathology
D000925:Anticoagulants; D006657:Histones; D010975:Platelet Aggregation Inhibitors