Key result
The absence of the EP3 receptor on platelets drastically reduced atherothrombosis induced by mechanical plaque rupture in mice compared to wild-type platelets, demonstrating that plaque-produced PGE2 exacerbates atherothrombosis.
Population
Mouse models of arterial thrombosis and atherosclerosis
Comparison
Platelets lacking EP3 receptor vs Platelets with intact EP3 receptor (wild-type)
Design
Preclinical
Authors
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EP3 inhibition on platelets merits investigation for atherothrombosis; animal findings leave open translation to human prevention.
Absolute Event Rate: 0.007% vs 0.16%
p-value: p=0.008
Inhibition of the platelet EP3 receptor may improve prevention of atherothrombosis by reducing PGE2-mediated platelet activation.
Gross et al. (2007) studied Arterial thrombosis and atherothrombosis. EP3 receptor deficiency vs. Wild-type (Ep3+/+) was evaluated on Extent of atherothrombosis induced by mechanical plaque rupture (x 10^6 pixels/min) (p=0.008). The absence of the EP3 receptor on platelets drastically reduced atherothrombosis induced by mechanical plaque rupture in mice compared to wild-type platelets, demonstrating that plaque-produced PGE2 exacerbates atherothrombosis.
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