Pulmonary vascular disease & thromboembolism
Targeting P2Y14 receptor (P2Y14R) alleviates platelet-induced neutrophil extracellular trap (NET) formation and venous thrombosis through PKA/AKAP13/RhoA axis
Authors' conclusion
Neutrophil P2Y14R deficiency regulates PKA/AKAP13/RhoA pathway to inhibit neutrophil-platelet aggregate, thereby reducing NET release and venous thrombosis.
Study context
- Population
- Venous thromboembolism (VTE) patients (P2Y14R expression); mouse models of DVT and disseminated intravascular coagulation
- Comparison
- Neutrophil-specific P2Y14R deficiency vs wild-type mice
Main finding
As reported in the abstract
- Neutrophil P2Y14R significantly increased in VTE patients
- Neutrophil-specific P2Y14R deficiency alleviated venous thrombosis and NET formation in mice
- P2Y14R deletion promotes PKA-induced AKAP13 phosphorylation, inhibiting RhoA activation and cytoskeleton rearrangement, reducing neutrophil-platelet aggregates and NET release
- Proglumide identified as potent P2Y14R antagonist; effect on thrombosis and NET formation verified
Original publication
Targeting P2Y14R alleviates platelet-induced NET formation and venous thrombosis through PKA/AKAP13/RhoA axis. Eur Heart J. Published 27 October 2025. doi:10.
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