ArticleEuropean heart journal2025
Reticulated platelets in coronary artery disease: a multidimensional approach unveils prothrombotic signalling and novel therapeutic targets.
Article in European heart journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Protection against postoperative atrial fibrillation via antiplatelet aggregation induced by remote ischemic preconditioning during off-pump coronary artery bypass grafting.Basic research in cardiology · 2026Trial
- Cardiac screening of amyloid TTR pathogenic variant carriers: complementary value of echocardiographic global longitudinal strain imaging and bone scintigraphy.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Article
- A transgenic mouse model for reticulated platelet detection reveals expansion after myocardial ischemia/reperfusion.Blood vessels, thrombosis & hemostasis · 2026Article
- Review
- The silent saboteurs: reticulated platelets in coronary artery disease.European heart journal · 2025Article
- The non-linear association between preoperative platelet to white blood cell ratio and 30-day postoperative mortality in adult tumor craniotomy: a retrospective cohort study.Frontiers in neurologyArticle
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Authors and funding
35 authors.
Funding
Abstract
BACKGROUND AND
aimsReticulated platelets (RPs), hyperreactive and RNA-rich, are associated with increased risk of cardiovascular events and suboptimal response to antiplatelet therapy in coronary artery disease (CAD). However, the underlying mechanisms remain poorly defined. This study aimed to characterize the molecular and functional phenotype of RPs in CAD and assess their potential as therapeutic targets.
methodsRPs and mature platelets (MPs) were isolated from CAD patients based on RNA content and CD41 expression. Paired RP vs MP comparisons were conducted within each donor. Transcriptomic profiling (RNA-seq) was integrated with high-dimensional proteomics (mass cytometry) and validated in independent cohorts. Functional studies, including flow cytometry-based platelet-platelet binding, in vitro thrombosis, platelet spreading, and intracellular phospho-protein profiling, assessed the impact of PI3K and GPVI pathways. Results were curated in Platlas, an open-access interactive web resource.
resultsAmong 95 CAD patients, RPs exhibited elevated activation marker expression and enrichment of prothrombotic pathways compared with MPs. RNA-seq revealed upregulation of GP6, TBXA2R, and VWF transcripts, novel GPVI splicing, and RP-specific non-coding RNAs including novel circRNAs. Proteomic and functional assays confirmed heightened PI3K and GPVI signalling, with increased phosphorylation of AKT, PI3K, and SYK, and elevated reactive oxygen species production. RPs showed increased aggregation, spreading and greater recruitment in thrombus formation, which were significantly reduced by PI3K (LY294002) and GPVI (glenzocimab) inhibition.
conclusionsThis 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.
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