Key result
P2Y12 deficiency significantly reduced neointima formation at 21 days after ferric chloride injury compared to control strain arteries (P<0.025).
Why the study?
Does P2Y12 deficiency reduce the vessel wall response to vascular injury and thrombosis in murine models?
Population
P2Y12-deficient (-/-) mice and littermate controls (+/+) on a C57 BL/6 background
Comparison
P2Y12 deficiency and bone marrow transplantation vs Wild-type littermate controls (+/+)
Design
Preclinical
Follow-up
21 days
Authors
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Implicates P2Y12 in post-injury vascular remodeling; hypothesis-generating for inhibition to limit restenosis, pending human data.
Does P2Y12 deficiency reduce the vessel wall response to vascular injury and thrombosis in murine models?
p-value: p=<0.025
Platelet P2Y12 receptor deficiency significantly reduces neointima formation and the vessel wall response to arterial injury in murine models, highlighting its role in atherogenesis and restenosis.
Evans et al. (2008) studied Arterial injury and thrombosis. P2Y12 deficiency vs. Littermate controls (+/+) was evaluated on Neointima formation at 21 days after ferric chloride injury (p=<0.025). P2Y12 deficiency significantly reduced neointima formation at 21 days after ferric chloride injury compared to control strain arteries (P<0.025).
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