Molecular Bad Actors and Thrombosis

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Abstract
The delicate balance of biochemical and cellular processes that the hemostatic mechanism comprises is dramatically highlighted by disorders that are provoked when one of the molecular components is missing or inactive. The number of participants in these processes is large and, to the dismay of nonspecialists, still growing in both quantity and complexity. The basic premise is that the procoagulant tendencies of the plasma proteins, platelets, and vascular surface are balanced by antithrombotic tendencies; yet the two opposing forces operating in concert possess the potential for a highly focal and limited response to injury that will help return the perturbed . . .