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Figure 1 | Journal of Intensive Care

Figure 1

From: Complement, thrombotic microangiopathy and disseminated intravascular coagulation

Figure 1

Crosstalks between coagulation, fibrinolysis and complement systems. The coagulation cascade is roughly divided into TF pathway and contact activation. The TF pathway is well known to get activated by TCC, trauma, and some cytokines. Both pathways will merge at FXa level, which will generate thrombin. Thrombin is one of the most potent activator of platelets. Upon platelet activation, medium-size polyphosphate in the platelet granules will be released, which can induce contact activation. FXIIa can activate the classical complement pathway. FXIIa can activate plasma kallikrein, which in turn can activate both C3 and C5. Other members of blood coagulation and fibrinolysis, such as FSAP, thrombin and plasmin can independently activate both C3 and C5. DAMPs, immune complex and PAMPs are known to activate the classical complement pathway. PAMPs and apoptotic cells will activate lectin pathway. PAMPs will trigger alternative pathway activation, all leading to C3 activation, which will activate C5. C3a and C5a will recruit and activate leukocytes, as well as induce platelet activation and aggregation, inducing thrombosis and inflammation, which are known to further enhance coagulation. C5b will lead to TCC formation, which not only lyse microorganisms but also lyse host cells, which will release DAMPs. TCC will induce TF pathway, induce platelet activation, and enhance coagulation by negatively charged phospholipid surfaces.

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