ABSTRACT
Introduction Unlike other cells, Figure 1 platelets lack a nucleus and therefore cannot adapt rapidly to their microenvironment with extensive de novo protein synthesis, although evidence for protein synthesis from mRNA in platelets has been described. 1 Thus, platelets need to be equipped with a sufficient supply of pre-existing molecules ready to react properly and efficiently within seconds to different (patho)physiological requirements. One of the predominant characteristics of platelets is the presence of a wide range of receptors, which are either constitutively expressed on the platelet surface or partially stored in storage granules and rapidly brought to the surface upon activation. Although the ‘original’ role of platelets is primary hemostasis, they express many receptors not directly involved in the thrombotic process. Thus, besides their role in hemostasis/thrombosis, platelets are significantly involved in various pathophysiological mechanisms, including inflammation, immunomodulation, tumor progression, and atherogenesis. 2-4 The border between physiological hemostasis and initiation or progression of diseases mediated by platelets is narrow and shifting. This chapter gives an overview of the central role of platelet receptors in platelet function, and focuses on their role receptors in atherothrombosis.
