Results: 2

1.
Figure 2

Figure 2. Proposed mechanisms for venous thrombosis.. From: New insights into the mechanisms of venous thrombosis.

My group proposed that formation of a venous thrombosis can be divided into distinct steps. First, the endothelium is activated by hypoxia and/or inflammatory mediators and expresses the adhesion proteins P-selectin, E-selectin, and vWF. Second, circulating leukocytes, platelets, and TF+ MVs bind to the activated endothelium. Third, the bound leukocytes become activated and express TF. The local activation of the coagulation cascade overwhelms the protective anticoagulant pathways and triggers thrombosis. The fibrin-rich clot also contains platelets and red blood cells.

Nigel Mackman. J Clin Invest. 2012 July 2;122(7):2331-2336.
2.
Figure 1

Figure 1. Activation of the coagulation cascade.. From: New insights into the mechanisms of venous thrombosis.

The coagulation cascade can be divided into the extrinsic (TF, FVIIa), intrinsic (FXIIa, FXIa, FIXa), and common (FXa and thrombin) pathways. The FIXa and FXa cofactors (FVIIIa and FVa, respectively) are not shown. Pathological activation of the extrinsic pathway is via TF expression in activated monocytes, monocyte-derived MVs, and possibly activated endothelial cells. Cellular RNA and polyphosphate (PolyP) released from activated platelets or bacteria activate FXIIa in the intrinsic pathway. The two new FDA-approved anticoagulant drugs rivaroxaban and dabigatran inhibit FXa and thrombin, respectively.

Nigel Mackman. J Clin Invest. 2012 July 2;122(7):2331-2336.

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