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Activated factor XIII (FXIIIa) crosslinks fibrin monomers to a stable clot. Due to this function, FXIIIa plays a major role in hemostasis and fibrinolysis. Additionally, it is well known that FXIIIa has a special meaning in cell adhesion and migration, in generation of extracellular matrix, in tissue repair and wound healing. New experimental studies revealed a FXIIIa stabilizing endothelial barrier function. In this function, FXIIIa reduces endothelial permeability for macromolecules in cultured endothelial monolayers and prevents impending barrier failure in coronary arteries of isolated hearts. This effect is due to the cross-linking of several proteins within the extracellular matrix, especially in the interendothelial clefts.

In addition to those wounds with increasing fragility of capillaries during impaired healing, there are especially long lasting diabetic wounds or calf ulcerations due to chronic venous insufficiency or postthrombotic syndrome that show a failure of endothelial barrier function with an increased permeability as an important part of its pathophysiological situation. The possibility of controlling this increased permeability is of great therapeutical interest and may give distinct benefit for wound healing. In the close past, clinical as well as experimental studies revealed the plasma transglutaminase (factor XIIIa) as potential new strategy in treatment of increased vascular permeability.