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Updated: Jun 4, 2026

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
Platelet function and antiplatelet therapy in cardiovascular disease: implications of genetic polymorphisms
Jayashree Shanker1, Armen Yuri Gasparyan, George D Kitas
1Thrombosis Research Institute, Bommasandra Industrial Area, Anekal Taluk, Bangalore, India. jayashreeshanker@triindia.org.in
Insights
Genetic variations in platelet receptors influence antiplatelet drug effectiveness. Analyzing these genetic polymorphisms may help personalize antiplatelet therapy and prevent cardiovascular events.
Area of Science:
- Pharmacogenomics
- Cardiovascular Medicine
- Hematology
Background:
- Platelets are key in thrombosis and cardiovascular diseases.
- Aspirin and clopidogrel are common antiplatelet drugs, but efficacy varies.
- This variability, termed 'antiplatelet resistance,' necessitates understanding underlying mechanisms.
Purpose of the Study:
- To investigate the role of genetic polymorphisms in platelet receptor genes.
- To explore the association between genetic variants and antiplatelet therapy response.
- To assess the potential for personalized antiplatelet treatment strategies.
Main Methods:
- Review of prospective studies on antiplatelet efficacy.
- Focus on genetic polymorphisms in platelet receptor genes (e.g., P2Y12, GP IIb/IIIa, CYP family).
- Consideration of genetic haplotypes and platelet function quantification.
Main Results:
- Specific genetic variants in platelet receptors are linked to variable responses to antiplatelet agents.
- Genetic polymorphisms and haplotypes can predict antiplatelet drug response.
- Combined genetic and platelet function testing may offer predictive value.
Conclusions:
- Genetic profiling of platelet receptors can inform antiplatelet therapy.
- Personalized antiplatelet treatment and thrombotic event prevention are potential benefits.
- Further research on cost-effectiveness of genetic and platelet function testing is required.
Abstract:
Platelets play a crucial role in thrombosis, inflammation, immunity and atherogenesis. Antiplatelet agents are widely used in patients with acute coronary syndrome and other cardiovascular disorders. Aspirin and clopidogrel are the most commonly prescribed antiplatelet agents, with a relatively safe profile and efficiency in a variety of clinical conditions. Numerous prospective studies have revealed variability of antiplatelet efficacy. The so called "antiplatelet resistance" prompted a search for mechanisms implicated in poor responsiveness to aspirin and clopidogrel therapy. In this regard, genetic polymorphisms in the platelet receptor genes attracted considerable interest. Specific genetic variants in platelet receptors such as the P2Y12, glycoprotein (GP) IIb/IIIa, GPIa/IIa, GPIb/IX/V and the cytochrome P450 (CYP) family of genes are associated with variable response to antiplatelet therapy and cardiovascular events. Genetic polymorphisms and haplotypes that comprehensively capture the genetic information encoded within the platelet receptor genes can, to some extent, predict response to the antiplatelet drug better than any single genotype. Genotyping for multiple receptor variants in patients on antiplatelet therapy, complemented by standardized quantification of platelet function, can provide useful information for future drug design studies and possibly for personalized antiplatelet therapy and prevention of thrombotic events. Additional information is, however, needed to evaluate the cost-effectiveness of complex genetic and platelet function testing.
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