Galectins as Novel Regulators of Platelet Signaling and Function: Therapeutic Implications

Abstract

Platelet activation at sites of vascular injury leads to the formation of a hemostatic plug. Activation of platelets is therefore crucial for normal hemostasis. However, uncontrolled platelet activation may also lead to the formation of occlusive thrombi that can cause ischemic events. Platelets can be activated by soluble molecules including thrombin, TXA2, ADP, serotonin or by adhesive extracellular matrix proteins such as von Willebrand factor and collagen. By acting either in soluble or immobilized form, Galectin-1 and 8 trigger platelet activation through modulation of discrete signaling pathways. These novel findings offer new hypotheses and some speculations about the role of platelet-galectin interactions not only in hemostasis and thrombosis but also in inflammation and related diseases such as atherosclerosis and cancer.