Key result
Blocking P2Y12 receptors or PI3Kbeta/gamma isoforms led to rapid disintegration of platelet aggregates, demonstrating that continuous signaling is required for dynamic thrombus stabilization.
Population
Human and murine thrombi formed on collagen under high shear conditions
Comparison
Blockade or suppression of P2Y12 receptors, PI3K… vs Unblocked/uninhibited state
Design
Preclinical
Authors
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May inform antiplatelet strategies targeting thrombus instability; leaves open translation from animal models to clinical use.
Continuous outside-in signaling via P2Y12 and PI3K beta/gamma isoforms is required to maintain platelet aggregate stability, suggesting a mechanism for dynamic thrombus instability relevant to antiplatelet therapy.
Cosemans et al. (2006) studied Thrombus formation. Blocking P2Y12 receptors or PI3K isoforms was evaluated on Thrombus disassembly. Blocking P2Y12 receptors or PI3Kbeta/gamma isoforms led to rapid disintegration of platelet aggregates, demonstrating that continuous signaling is required for dynamic thrombus stabilization.
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