Background: Platelet hyperactivity has been implicated in many cardiovascular (CV) events such as
ischemic stroke, myocardial infarction and CV death. Genetic variability of platelet receptors has been shown to
impact Src family kinases (SFKs) activation and in turn influence platelet activation. SFKs are important signal
transmitters in platelets, interacting with several receptors as GPIIB/IIIa, GPIb, PEAR 1, GPIa, GPVI, PECAM
Methods: In this review, we focused on genetic variants of platelet receptors whose signals are transmitted
mainly by SFKs and may be associated with clinical manifestations of platelet hyperactivation like MI or IS.
Results: The genetic variants of platelet receptors, the signals of which are transmitted by SFKs, and the associated
clinical manifestations in platelet hyperactivation, have been examined. The most extensively studied receptors
were glycoprotein polymorphisms. The greatest numbers of genetic variants were analyzed in GPIb.
GPIIb/IIIa receptor polymorphisms were also well analyzed and many studies highlighted their associations with
ischemic stroke (IS) and myocardial infarction (MI). However, there are a number of conflicting studies finding
that GPIIb/IIIa receptor polymorphisms may not influence platelet hyperactivity. Moreover, variability within
some other receptors like GPVI, PECAM, PEAR1, and CD148 was analyzed only in single studies.
Conclusions: Src family kinases are one of the most important signal transmitters in platelets. Some receptors
have well documented interactions with SFKs, while other have not been examined in humans or data about its
association originated from single studies. Further studies are necessary to confirm the findings and reduce falsepositive