ArticleResearch and practice in thrombosis and haemostasis2026
Comparison of variably specific Bruton tyrosine kinase inhibitors on platelet aggregation mediated by Fcγ receptor (FcγR) IIa, glycoprotein VI, and platelet endothelial aggregation receptor (PEAR) 1: implications for Bruton tyrosine kinase inhibitors as antithrombotic therapy.
Article in Research and practice in thrombosis and haemostasis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Bruton tyrosine kinase (BTK) inhibitors (BTKi) have been proposed as therapy for thrombosis driven by immune complex activation of platelets via FcγRIIa. Since patients who lack BTK (X-linked agammaglobulinemia [XLA]) do not have excessive bleeding, highly specific BTKi may be antithrombotic without increasing the risk of hemorrhage. Our knowledge of the full range of effects of BTKi on platelet function is incomplete, in particular, the role of BTKi on signaling via platelet endothelial aggregation receptor (PEAR) 1, a receptor linked to thrombotic cardiovascular disease. Objectives: This study assessed the role of BTK in platelet aggregation initiated through Fcγ receptor (FcγR)IIa, glycoprotein (GP)VI, PEAR1, and other receptors. Methods: Platelets of control and patients with XLA were treated with BTKi of varying specificity and analyzed by light transmission aggregometry and immunoblotting. Results: Both nonspecific and highly specific BTKi profoundly inhibited platelet aggregation mediated by FcγRIIa, PEAR1, and GPVI, but not protease-activated receptor 1, the thromboxane receptor, α Conclusion: BTK plays important roles in signaling via FcγRIIa, GPVI, and PEAR1, but clinical studies are required to assess the optimal BTKi for inhibiting thrombotic disorders mediated via these receptors.
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