Coronary disease & ACSMechanistic study
Reticulated platelets in coronary artery disease: a multidimensional approach unveils prothrombotic signalling and novel therapeutic targets
- Mechanistic study
- paired within-donor comparison
- validated in independent cohorts
Authors' conclusion
This study provides the first mechanistic explanation for RP hyperreactivity, revealing a distinct molecular profile and identifying GPVI and PI3K inhibition as promising targets for tailored antiplatelet therapy in CAD patients with elevated RPs.
Study context
- Population
- Patients with coronary artery disease (CAD)
- Participants
- 95 patients
- Comparison
- Reticulated platelets vs mature platelets
Main finding
As reported in the abstract
Molecular and functional phenotype of RPs vs MPs (paired, within donor)
- Reticulated platelets (RPs): elevated activation marker expression and enrichment of prothrombotic pathways vs mature platelets (MPs)
- RNA-seq: upregulation of GP6, TBXA2R and VWF transcripts, novel GPVI splicing, RP-specific non-coding RNAs incl. novel circRNAs
- Heightened PI3K and GPVI signalling: increased phosphorylation of AKT, PI3K and SYK, elevated reactive oxygen species production
- RPs: increased aggregation, spreading and greater recruitment in thrombus formation, significantly reduced by PI3K (LY294002) and GPVI (glenzocimab) inhibition
- 95 CAD patients
Original publication
Reticulated platelets in coronary artery disease: a multidimensional approach unveils prothrombotic signalling and novel therapeutic targets. Eur Heart J. Published 31 August 2025. doi:10.1093/eurheartj/ehaf694
Summarised from the published abstract; every number is checked against it