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炎症、先天免疫和血液凝固。

Inflammation, innate immunity and blood coagulation.

机构信息

Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.

出版信息

Hamostaseologie. 2010 Jan;30(1):5-6, 8-9.

Abstract

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.

摘要

炎症可导致动脉、静脉和微血管血栓形成。慢性炎症可导致动脉血栓并发症,而急性炎症则会导致静脉血栓和微血管血栓形成。从机制上讲,炎症通过上调促凝物、下调抗凝物和抑制纤维蛋白溶解来调节血栓反应。炎症反应还可导致细胞凋亡或坏死。从死亡细胞中释放的产物,特别是组蛋白,会引发进一步的炎症、组织死亡和器官衰竭。抑制组蛋白介导的细胞毒性似乎是防止这种致命级联反应的一种新机制。

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