Inflammation-Induced Thrombosis: Mechanisms, Disease Associations and Management
Makaleler > Derleme · 2012
Yazarlar: Kenan AKSU, Ayhan DÖNMEZ, Gökhan KESER
CURRENT PHARMACEUTICAL DESIGN, SCI Expanded İndekslerine Giren Dergi, Uluslararası, 2012, cilt 18, ss 1478-1493
Özet
Although inflammation-induced thrombosis is a well-known entity, its pathogenesis remains complicated. There are complex interactions between inflammation and hemostasis, involving proinflammatory cytokines, chemokines, adhesion molecules, tissue factor expression, platelet and endothelial activation, and microparticles. Inflammation increases procoagulant factors, and also inhibits natural anticoagulant pathways and fibrinolytic activity, causing a thrombotic tendency. Besides, chronic inflammation may cause endothelial damage, resulting in the loss of physiologic anticoagulant, antiaggregant and vasodilatory properties of endothelium. However, inflammation-induced venous thrombosis may develop even in the absence of vessel wall damage. On the other hand, coagulation also augments inflammation, causing a vicious cycle. This is mainly achieved by means of thrombin-induced secretion of proinflammatory cytokines and growth factors. Platelets may also trigger inflammation by activating the dendritic cells.