A crucial aspect of hemostasis in mammals is the control of the formation and dissolution of a fibrin matrix. The enzymatic system in plasma for fibrin formation consists of more than a dozen proteases and cofactors that act in series (Jackson and Nemerson 1980). Localization of these reactions is achieved by the requirement for the phospholipid surface, which is supplied by activated platelets at the site of trauma. Regulation of fibrin formation is achieved through control of protease activation, the requirement for a phospholipid surface at certain steps of the cascade, and feedback activation and inactivation reactions involving coagulation factors, other plasma proteins, and cell-surface proteins. The resulting fibrin matrix serves to prevent unwanted blood loss at the site of an injury.
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Vehar et al. (1986) studied this question.