Warwick Scott Nesbitt

TL;DR: High-resolution intravital imaging techniques and hydrodynamic analyses show that platelet aggregation is primarily driven by changes in blood flow parameters (rheology), with soluble agonists having a secondary role, stabilizing formed aggregates.

TL;DR: This study has defined a key role for the Type Ia phosphoinositide 3-kinase (PI3K) p110β isoform in regulating the formation and stability of integrin αIIbβ3 adhesion bonds, necessary for shear activation of platelets, as an important new target for antithrombotic therapy.

TL;DR: This review will discuss the major platelet adhesive interactions regulating platelet thrombus formation under high shear, with specific focus on the VWF and collagen receptors and the signaling mechanisms utilized by these receptors to induce platelet activation.

TL;DR: Unraveling the dynamics of platelet aggregation and thrombus formation in vivo requires consideration of the cooperative interplay between rheological‐ and soluble agonist‐dependent Platelet aggregation mechanisms.

TL;DR: A new mechanism initiating platelet aggregation that is critically influenced by shear, physical proximity between translocating platelets, and membrane tether formation is identified and a model to explain how the discoid morphology of platelets facilitates the maintenance of adhesive interactions with thrombogenic surfaces under high shear stress conditions is provided.