Figure 1.
Mechanisms of classical hemostasis after traumatic vessel injury. (A) Traumatic injury leads to exposure of extracellular matrix (ECM) proteins, such as collagen and binding of von Willebrand factor (vWF) derived from endothelial cells and platelets. Adhesion of incoming platelets to the injured vessel wall is mediated by the vWF-binding glycoprotein GPIbα. (B) Activation of recruited platelets and distinct shape change through auto- and paracrine secretion of prothrombotic factors, such as adenosine 5′-diphosphate, leading to an increased affinity of the αIIbβ3/GPIIBIIIA receptor. (C) Binding of fibrinogen activates integrin inside-out signaling pathways, thus promoting aggregation of neighboring platelets and resulting in a stable thrombus formation.

Mechanisms of classical hemostasis after traumatic vessel injury. (A) Traumatic injury leads to exposure of extracellular matrix (ECM) proteins, such as collagen and binding of von Willebrand factor (vWF) derived from endothelial cells and platelets. Adhesion of incoming platelets to the injured vessel wall is mediated by the vWF-binding glycoprotein GPIbα. (B) Activation of recruited platelets and distinct shape change through auto- and paracrine secretion of prothrombotic factors, such as adenosine 5′-diphosphate, leading to an increased affinity of the αIIbβ3/GPIIBIIIA receptor. (C) Binding of fibrinogen activates integrin inside-out signaling pathways, thus promoting aggregation of neighboring platelets and resulting in a stable thrombus formation.

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