Figure 1.
Figure 1. Mononuclear cells express tissue factor resulting in thrombin generation and subsequent fibrinogen to fibrin conversion, which, in combination with increased platelet vessel wall interaction and activation of platelets, contribute to microvascular clot formation. P-selectin released from activated platelets further upregulates tissue factor expression. Binding of fibrin to Toll-like receptor 4 and activated coagulation proteases to specific protease activated receptors (PARs) on inflammatory cells (dotted lines) modulates inflammation through the additional release of proinflammatory cytokines. Cytokines also play a key role in the suppression of endogenous fibrinolysis and impairment of physiological anticoagulant pathways, such as the APC pathway.

Mononuclear cells express tissue factor resulting in thrombin generation and subsequent fibrinogen to fibrin conversion, which, in combination with increased platelet vessel wall interaction and activation of platelets, contribute to microvascular clot formation. P-selectin released from activated platelets further upregulates tissue factor expression. Binding of fibrin to Toll-like receptor 4 and activated coagulation proteases to specific protease activated receptors (PARs) on inflammatory cells (dotted lines) modulates inflammation through the additional release of proinflammatory cytokines. Cytokines also play a key role in the suppression of endogenous fibrinolysis and impairment of physiological anticoagulant pathways, such as the APC pathway.

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