February 2017

A team of DZHK researchers led by Prof. Dr. Philip Wenzel from the Rhein-Main partner site have discovered a previously unknown interaction between factors of blood coagulation and inflammatory response and report their findings in Science Translational Medicine. They were able to prove that activation of a blood coagulation factor known as factor XI is higher in patients with arterial hypertension. By blocking factor XI, it was possible to significantly lower blood pressure, and fewer inflammatory responses occurred. In the context of their study the research team administered angiotensin II­, a hormone which causes an increase in blood pressure, to an animal model. This triggers an inflammatory response in the blood vessel wall which is significantly enhanced by components of the blood coagulation system. The investigators found out that blood coagulation factor XI is responsible for the increased inflammatory response. The real task of factor XI is to stimulate the activation of coagulation on the surface of the blood platelets. It is supported in this task by surface receptors on the platelets. Inhibition of this coagulation factor, which plays only a minor role in normal hemostasis, was even able to markedly reduce kidney damage. Patient specimens also showed clear evidence of increased coagulation activation on blood platelets in patients with elevated blood pressure. Here, too, blood coagulation factor XI was the key driver. These findings suggest that drug-induced inhibition of factor XI could benefit patients with high blood pressure. 

Link