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- W4387157828 abstract "Inflammation is a complex pathophysiological process underlying many clinical conditions. Platelets contribute to the thrombo-inflammatory response. Platelet P2Y12 amplifies platelet activation, potentiating platelet aggregation, degranulation and shape change. The contents of platelet alpha granules in particular act directly on leucocytes, including mediating platelet-leucocyte aggregation and activation via platelet P-selectin. Much evidence for the role of platelet P2Y12 in inflammation comes from studies of P2Y12 inhibitors such as the thienopyridines clopidogrel and prasugrel, and the cyclopentyltriazolopyrimidine ticagrelor, including in animal and human experimental models. These suggest P2Y12 inhibition reduces markers of inflammation with some evidence this reduces incidence of adverse clinical sequelae during inflammatory conditions. Interpretation is complicated by pleiotropic effects such as of thienopyridines on circulating leucocyte numbers and of ticagrelor on adenosine reuptake. The available evidence suggests P2Y12 as a prominent mediator of inflammation and P2Y12 inhibition as a potentially powerful strategy in a broad range of inflammatory conditions." @default.
- W4387157828 created "2023-09-30" @default.
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- W4387157828 date "2023-09-28" @default.
- W4387157828 modified "2023-09-30" @default.
- W4387157828 title "THE ROLE OF PLATELET P2Y<sub>12</sub> IN INFLAMMATION" @default.
- W4387157828 doi "https://doi.org/10.1111/bph.16256" @default.
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- W4387157828 hasPublicationYear "2023" @default.
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