| |
[摘要]：In this issue of Blood, May and colleagues(1) demonstrate that the recently described platelet receptor CLEC-2 is important for stabilizing platelet cohesion and thrombus development under flow conditions. The absence of CLEC-2 in vivo is manifested by a continuous release of individual platelets from the growing thrombus and the embolization of small platelet aggregates, resulting in impaired occlusion of damaged vessels in CLEC-2-deficient mice. |
|
