Cardiovascular diseases are still among the most common causes for morbidity and mortality in industrialised countries. They become manifest in coronary heart disease, myocardial infarction, ischaemic stroke, but also in deep vein thrombosis and pulmonary embolism. Usually there are several underlying risk factors present such as obesity, diabetes, increased blood lipids, smoking, and a sedentary lifestyle, causing damage to blood vessels and promoting the development of atherosclerosis. This leads to inflammatory processes within the vessel wall and a procoagulant state. When blood coagulation is triggered a blood clot forms which can partially or completely occlude the affected blood vessel. Our research group is interested in the procoagulant changes and mechanisms that lead to formation of blood clots. One focus of our work is coagulation factor XIII (FXIII). During coagulation FXIII becomes activated by thrombin and, as a transglutaminase, crosslinks loose fibrin fibres to a stable fibrin network, thus FXIII crucially contributes to clot formation. We study the role of FXIII in cardiovascular diseases, characterise mutations causing congenital FXIII deficiency, and perform biochemical studies to investigate the role of FXIII activation peptide using functional assays and cell expression of FXIII variants. Another focus of our work is the complement system, a part of the immune system which is involved in the inflammatory processes in vascular diseases. We study interactions between the complement system and blood coagulation that promote clot formation and increase the risk of thrombotic events.