GEO series
Inhibiting the P2Y12 Receptor in Megakaryocytes and Platelets Suppresses Interferon-Associated Responses
GSE242369
Homo sapiens
Expression profiling by high throughput sequencing
19 samples
2025/05/07
GPL24676
Summary
Megakaryocytes (MKs) and platelets are recognized mediators of inflammation and altered immunity. While antiplatelet therapies are widely used to prevent cardiovascular events, their role in attenuating platelet-mediated inflammation is uncertain. This study was designed to investigate the transcriptomic effect of APT on MKs and its impact on proinflammatory pathways. We demonstrated a significant effect on the MK transcriptome following P2Y12 receptor inhibition. Specifically, we found a significant downregulation of IFN pathways with P2Y12 receptor inhibition. In conclusion, targeting the P2Y12 receptor modulates MK and platelet inflammatory signaling pathways. P2Y12-mediated suppression of MK IFNα signaling may benefit proinflammatory diseases
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Paper (PMID 39444926) ↗
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