Abstract

 Background and Objectives

 Platelets are the smallest blood cells which play a major role in hemostasis. The aim of this article is to investigate the most effective cell adhesions and the most important signaling pathways to activate or deactivate platelets at the site of vessel injury.

 Materials and Methods

 The present manuscript, using 52 recent published articles, introduces the latest information regarding the platelet molecular interactions and signaling pathways.

 Results

 Platelets at the site of vessel injury bind to the subendothelial extracellular matrix through their surface receptors. These interactions lead to activation of some intracellular pathways contributing to the formation of blood clots. The molecules involved in these interactions are the extracellular matrix molecules such as laminin, fibronectin, collagen, vWF and the platelet surface receptors such as GPVI, GPIb-V-IX, α IIbβ3 and α2β1 integrins. Platelet functions in hemostasis, thrombosis and inflammation are directly attributed to the platelet-cell interactions, cell junctions and the signaling pathways regulated through these interactions.

 Conclusions

 Studying this field and the related mechanisms provides a better understanding of coagulation and platelet dependent hematologic diseases, and may offer new perspectives to immunogenic disorders.