Why the study?
Does alpha(2A)-adrenergic receptor deficiency reduce thrombus stability in mouse models of thrombosis?
Population
alpha(2A)-deficient mice and wild-type mice
Comparison
alpha-adrenergic receptor deficiency vs Wild-type mice
Design
Preclinical
Key result
Alpha2A-adrenergic receptor deficiency in mice resulted in reduced thrombus stability, with 24% of deficient mice showing embolization and reestablished blood flow compared to 0% of wild-type mice.
Authors
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Alpha2A-adrenergic receptor modulates thrombus stability in mice; leaves open whether this pathway is a viable human antithrombotic target.
Does alpha(2A)-adrenergic receptor deficiency reduce thrombus stability in mouse models of thrombosis?
Absolute Event Rate: 76% vs 100%
The alpha(2A)-adrenergic receptor plays a significant role in in vivo thrombus stabilization, as its deficiency in mice leads to increased embolization and reduced irreversible occlusion.
Požgajová et al. (2006) studied Thrombosis. alpha2A-adrenergic receptor deficiency vs. Wild-type mice was evaluated on Irreversible vessel occlusion following mechanical injury. Alpha2A-adrenergic receptor deficiency in mice resulted in reduced thrombus stability, with 24% of deficient mice showing embolization and reestablished blood flow compared to 0% of wild-type mice.
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