Role of defensins in immunothrombosis

The interaction between innate immunity and coagulation is essential in thrombotic diseases, but the molecular links remain unclear. Neutrophils are key players, releasing mediators such as defensins, which are small cationic peptides with antimicrobial functions. Defensins contribute to platelet activation and the formation of neutrophil extracellular traps. This review examines the mechanistic role of defensins in immunothrombosis, focusing on their effects on platelet activation, fibrinolysis, and endothelial function. We also discuss their involvement in autoimmune diseases, such as systemic lupus erythematosus and antiphospholipid syndrome, and evaluate defensins as potential therapeutic targets. α‐ and β‐defensins may serve as biomarkers for thrombotic risk in coronary artery disease, coronavirus disease 2019, and sepsis. Mechanistically, defensins impair clot dissolution, enhance platelet aggregation, and disrupt the von Willebrand factor/ADAMTS13 balance. Colchicine reduces defensin‐mediated thrombosis by inhibiting neutrophil degranulation, suggesting a promising treatment strategy. Targeting defensin offers a potential therapeutic approach for managing thrombotic complications in inflammatory and autoimmune diseases.