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Updated: May 23, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Platelet proteome and clopidogrel response in patients with stable angina undergoing percutaneous coronary
Elisabetta Volpi1, Laura Giusti, Federica Ciregia
1Scuola Superiore Sant'Anna, Pisa, Italy. volpi@ifc.cnr.it
Insights
Clopidogrel therapy significantly reduced platelet activation markers in stable angina patients. Proteomic analysis revealed changes in proteins related to cytoskeleton, metabolism, and oxidative stress, offering insights into clopidogrel response.
Area of Science:
- Cardiovascular Medicine
- Proteomics
- Pharmacology
Background:
- Platelet reactivity is crucial in stable angina patients undergoing percutaneous coronary intervention (PCI).
- Understanding clopidogrel response mechanisms is vital for optimizing antiplatelet therapy.
Purpose of the Study:
- To investigate platelet proteome changes during early clopidogrel therapy in stable angina patients post-PCI.
- To explore mechanisms controlling platelet reactivity and clopidogrel response.
Main Methods:
- Proteomic analysis of circulating platelets from 20 patients at baseline, 12h, and 24h after clopidogrel loading.
- Assessment of platelet reactivity using flow cytometry and aggregation tests.
Main Results:
- Clopidogrel loading dose significantly inhibited platelet activation markers.
- MS/MS identified 18 differentially expressed proteins involved in cytoskeleton rearrangement, energy metabolism, and oxidative stress.
Conclusions:
- Novel insights into platelet proteome alterations related to clopidogrel therapy and platelet activation.
- Highlights the potential of proteomic studies for identifying new platelet biomarkers.
Objectives:
We analyzed the platelet proteome of circulating platelets during the onset of clopidogrel therapy in patients with stable angina underwent percutaneous coronary intervention in order to investigate the mechanisms that control platelet reactivity and clopidogrel response in this context.
Design & Methods:
Twenty patients were enrolled in this study. Blood samples were collected before coronary angiography (T0), 12 h after 600 mg of clopidogrel (T1) and 24 h after percutaneous coronary intervention (PCI) (T2). Platelet reactivity, Clopidogrel response and proteomic analysis were examined.
Results:
Clopidogrel loading dose produced a significant inhibition in all markers of platelet activation in both flow cytometry and aggregation tests. Among the proteins found differentially expressed, eighteen were identified by MS/MS analysis and they resulted involved in the cytoskeleton rearrangement (profilin-1, calpain, α-soluble NSF attachment protein, thrombospondin), in the energetic metabolism (ubiquitin-like modifier-activating enzyme 1, protein-L-isoaspartate-(D-aspartate) O-methyltransferase and nucleoside diphosphate kinase B) and in the oxidative stress (heat shock 70 kDa protein 5 and anti-stress induced phosphoprotein 1.
Conclusions:
The present study provides novel information on platelet proteome changes associated with platelet activation and clopidogrel response. This investigation supports the development of further proteomic studies for the identification of novel platelet biomarkers.
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