Disseminated thrombotic process in the microcirculation is considered to be an important cause of multiple organ dysfunction in sepsis. The fundamental purpose of this prothrombotic change was believed to be in the host defense against microbial dissemination. In that process, antifibrinolytic property plays an important role.
For the understanding of pathophysiology of sepsis, it is quite useful to grasp the alterations in coagulation/fibrinolytic parameters, i.e., plasminogen activator and plasminogen activator inhibitor-1. They play crucial roles in the development of clot formation and disseminated intravascular coagulation that leads to fatal organ dysfunction. Basically, fibrinolysis is a simple system compared to the complex coagulation cascade. Plasmin is the only factor that regulates fibrinolysis, and this enzyme is modulated by several factors including plasminogen activators and plasminogen activator inhibitor-1. However, recent studies have elucidated the complex regulation of the production, activation, and inactivation of these fibrinolytic factors.
The dynamic change of the fibrinolytic system plays a crucial role in the pathophysiology of sepsis. In this commentary, we introduce the recent advances of the research regarding fibrinolytic system.