Vessel-blocking thrombus formation (white) in damaged mesenteric vessels is prevented in the absence of coagulation factor XII (bottom panels).

On page 271, Renné and colleagues show that the absence of a clot-promoting protein in mice keeps arteries from clogging with no risk of excessive bleeding. These data challenge the decades-old belief that this protein—called factor XII (FXII) or Hageman factor—has no impact on clotting in vivo.

Blood clotting depends on the sequential activation of proteins, called clotting factors, that culminates in the production of fibrin—the protein that forms the meshwork of the clot. This process must be tightly regulated, as too little clotting can lead to bleeding disorders and too much clotting can lead to blood vessel blockage, which triggers strokes and heart attacks.

Deficiencies in some blood clotting proteins, such as tissue factor and factor VII, result in fatal bleeding disorders. But deficiencies...

You do not currently have access to this content.