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Sepsis causes fibrinolytic insufficiency due to low plasminogen, leading to microvascular thrombosis. Plasminogen supplementation shows promise for treating this sepsis-induced coagulopathy.

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Area of Science:

  • Coagulation and Fibrinolysis
  • Immunothrombosis
  • Sepsis Pathophysiology

Background:

  • Sepsis disrupts the balance between coagulation and fibrinolysis, leading to microvascular thrombosis, organ failure, and mortality.
  • While initial fibrinolysis may increase, it's overcome by plasminogen activator inhibitor-1 (PAI-1) and other factors, causing fibrinolytic insufficiency.
  • Emerging evidence highlights a quantitative defect in plasminogen as a key contributor to impaired fibrinolysis in sepsis.

Purpose of the Study:

  • To investigate the role of plasminogen deficiency in sepsis-induced fibrinolytic insufficiency.
  • To explore the link between neutrophil extracellular traps (NETs) and plasminogen dysfunction.
  • To evaluate plasminogen supplementation as a potential therapeutic strategy for sepsis-related coagulopathy.

Main Methods:

  • Analysis of the NET-plasminogen axis and its impact on fibrinolysis.
  • Clinical characterization of hypofibrinolysis using biomarkers (D-dimers, PAI-1) and viscoelastic testing.
  • Translational studies involving plasminogen supplementation in septic patients and experimental DIC models.

Main Results:

  • Neutrophil elastase in NETs cleaves plasminogen, reducing functional availability and impairing fibrinolysis.
  • Low functional plasminogen leads to persistent fibrin deposition despite elevated D-dimer levels.
  • Plasminogen supplementation restored functional plasminogen and normalized plasmin generation in experimental models and septic patients.

Conclusions:

  • The NET-plasminogen axis is a critical factor in sepsis-induced coagulopathy and disseminated intravascular coagulation (DIC).
  • Hypofibrinolysis in sepsis is characterized by high D-dimers, elevated PAI-1, and reduced plasmin generation.
  • Plasminogen supplementation offers a promising therapeutic approach to restore fibrinolytic balance in sepsis.