Key result
Cyclosporin A and Ru360 inhibit a novel supramaximal calcium signal to prevent procoagulant platelet formation.
Why the study?
Procoagulant platelets promote thrombin generation during thrombosis in an all-or-nothing manner, but how distinct Ca2+ signaling commits specific platelet subpopulations to become procoagulant was unclear.
Population
Platelets
Comparison
Fluo-4 vs Fluo-5N indicators and treatment with cyclosporin A, Ru360, or Synta-66
Design
In vitro experimental study
Authors
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May offer novel antithrombotic targets via mitochondrial calcium inhibition; leaves open translation to human thrombosis prevention.
Procoagulant platelets require a distinct, supramaximal calcium signal dependent on mitochondrial pathways, offering potential new targets to limit thrombosis.
Abbasian et al. (2020) studied Thrombosis. Cyclosporin A, Ru360, and Synta-66 was evaluated on Cytosolic Ca2+ concentrations and percentage of procoagulant platelets. Procoagulant platelets exhibit a novel supramaximal calcium signal that is inhibited by cyclosporin A and Ru360, providing new targets to prevent procoagulant platelet formation.
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