Figure 8

Proposed mechanism of erythrocyte contribution to vascular occlusion via VWF binding. Upon cellular stress, erythrocytes show deformation, shrinkage and exposition of phosphatidylserine (PS) as well as Annexin V (AV). Intravascular VWF of activated endothelium binds surface AV of these stressed erythrocytes, whereas unstressed, vital erythrocytes do not adhere. Although this binding is mainly reversible, it can still lead to an impairment of dynamic blood flow and vascular occlusion. This binding can be blocked by anti-AV antibody, heparin and ADAMTS13.