ArticleJournal of cellular physiology2026
Distinct Thromboxane A₂-Dependent Pathways Regulate Arachidonic Acid-Triggered VASP Phosphorylation at Ser239 and Ser157 in Human Platelets: Real-Time Visualization Reveals Superior Antithrombotic Efficacy by Targeting Thromboxane A₂ Signaling over Cyclooxygenase Inhibition.
Article in Journal of cellular physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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7 authors.
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Abstract
Platelets, as anucleate blood cells, play a pivotal role in the pathogenesis of cardiovascular diseases (CVDs), making antiplatelet therapy essential for preventing thrombotic events such as myocardial infarction. Thromboxane A₂ (TXA₂) is a key pro-aggregatory mediator that drives platelet activation. Phosphorylation of vasodilator-stimulated phosphoprotein (VASP) at Ser157 and Ser239 serves as a marker of cyclic nucleotide-mediated inhibitory signaling. The crosstalk between TXA₂ signaling and site-specific VASP phosphorylation in arachidonic acid (AA)-stimulated human platelets remains unclear and requires further investigation. In this study, AA at 60 µM induced maximal platelet activation, as evidenced by ultrastructural changes and increased P-selectin expression. Picotamide, a thromboxane synthase (TXS) inhibitor, effectively reversed AA-induced alterations, including ultrastructural remodeling, P-selectin expression, TXA₂ production, adenosine triphosphate (ATP)-release, mobilization of [Ca²⁺]ᵢ, and integrin α
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