ArticleThrombosis research2013
Pharmacodynamic interplay of the P2Y(1), P2Y(12), and TxA(2) pathways in platelets: the potential of triple antiplatelet therapy with P2Y(1) receptor antagonism.
Article in Thrombosis research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Effect of genetic variation in P2Y12 on TRAP-stimulated platelet response in healthy subjects.Journal of thrombosis and thrombolysis · 2014Trial
- A Perspective on How Fibrinaloid Microclots and Platelet Pathology May be Applied in Clinical Investigations.Seminars in thrombosis and hemostasis · 2024Review
- ADP-Mediated Upregulation of Expression of CD62P on Human Platelets Is Critically Dependent on Co-Activation of P2Y1 and P2Y12 Receptors.Pharmaceuticals (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
introductionPrevious work suggests that the extent of platelet inhibition by P2Y(1) receptor antagonism may be underappreciated, particularly in the context of dual antiplatelet therapy with aspirin and clopidogrel. MATERIALS AND
methodsUsing P2Y(1), P2Y(12), and TxA(2) receptor antagonists individually and in combination, we assessed the incremental changes from baseline platelet reactivity in blood collected from healthy volunteers.
resultsThe P2Y(1) receptor antagonist further inhibited platelet activation and aggregation in several assay conditions ex vivo when combined with P2Y(12) and/or TxA(2) receptor blockers. Collagen and TRAP-induced platelet aggregation measured by light transmittance aggregometry was inhibited to a greater extent with the triple combination relative to each of the antagonists alone. The triple combination of P2Y(1), P2Y(12), and TxA(2) receptor antagonists also significantly shifted adenosine diphosphate (ADP)-stimulated platelet glycoprotein IIb/IIIa receptor and P-selectin expression compared to individual or dual antagonists.
conclusionsThese results substantiate that additional platelet inhibition occurs with the triple combination of P2Y(1), P2Y(12), and TxA(2) receptor antagonists and support further testing of P2Y(1) receptor antagonists as an option for alternative, synergistic, or triple antiplatelet therapy.
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