The platelet glycoprotein V is an important switching point for hemostasis and thrombus formation. This new finding could have great clinical potential.
If our blood vessels are injured by cuts or abrasions or bruises, it is vital that the bleeding is stopped and the wound closed. In technical terms, this process is called hemostasis. This consists of two processes: the hemostasis, in which platelets (platelets) attach to the wound edges, form a plug and temporarily seal the injury. And the blood clotting or coagulation cascade, in which long fibers are formed from fibrin, which together with the platelets seal the wound firmly.
However, if fibrin is formed in excess, for example in chronic wounds, vascular occlusions, so-called thrombosis, can occur. Strict regulation of fibrin formation is therefore important. However, how coagulation is limited has not yet been fully understood.
In an international project coordinated by Würzburg University Medicine, researchers have now deciphered a central regulatory mechanism for fibrin formation and derived new therapeutic approaches from it. The results are released in the renowned journal Nature Cardiovascular Research.