The Thromboinflammation Group investigates how inflammatory, vascular, and haemostatic pathways interact during acute tissue injury to shape microvascular function and organ outcome. Our work focuses on the mechanisms by which injury-induced inflammation and coagulation become mutually reinforcing, forming thromboinflammatory circuits that can either facilitate controlled repair or escalate into microvascular dysfunction and organ failure. By dissecting these coupled responses, we aim to establish mechanistic biomarkers and develop targeted interventions for trauma, haemorrhage, and transfusion-associated injury.
Acute injury triggers rapid and tightly coordinated activation of immune, endothelial, and coagulation systems. Rather than functioning as separate entities, these pathways form an integrated network that governs vascular integrity, intravascular inflammation, fibrin deposition, and tissue regeneration. To unravel this complexity, the Thromboinflammation Group combines advanced in vitro and ex vivo platforms with high-resolution analysis of inflammatory–haemostatic communication. Complementary in vivo studies provide essential physiological context to interrogate multi-organ interactions and evaluate therapeutic strategies. Our models span modular murine systems of tissue trauma, haemorrhage, and combined injuries (thoracic, hepatic, skeletal), as well as large-animal models that capture clinically relevant coagulopathy and enable translational testing.