Activation of the Plasma Contact System Triggers the Fat Embolism Syndrome

Sandra Konrath, M.Sc.
University Medical Center Hamburg-Eppendorf (UKE)
Hamburg, Germany

Fat embolism syndrome (FES) is a rare but severe thromboinflammatory complication occurring after fractures of long tubular bones with subsequent release of lipids from the bone marrow into circulation. Its mechanism is poorly understood, and targeted therapy remains to be developed. In this presentation, Sandra Konrath focuses on the potential of bone marrow (BM)-derived lipids to activate the procoagulant and proinflammatory factor XII (FXII)-driven plasma contact system that mediates the pathogenesis of FES. In vitro studies showed that BM-derived lipids trigger clotting in plasma in a FXII-dependent manner. To assess the prothrombogenic activity of BM-derived lipids in vivo, results of a lethal pulmonary embolism model in wild-type mice and animals with genetic deficiency in FXII will be discussed.

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