Background: Platelets are an important link between inflammation, thrombosis, and atherogenesis. Inflammation is characterized by interactions among platelets, leukocytes, and endothelial cells. These interactions trigger autocrine and paracrine activation processes that lead to leukocyte recruitment into the vascular wall. Platelet-induced chronic inflammatory processes at the vascular wall result in development of atherosclerotic lesions and atherothrombosis.
Methods: In vitro studies with co-incubated human endothelial cells and platelets after physical denudation or activation of the endothelium by cytokines provided important results for the understanding of adhesion mechanisms and the involvement of different adhesion receptors, like integrins and selectins. Furthermore, in in vivo mouse models platelet-endothelium interactions under dynamic flow conditions and increased shear stress could be analyzed. With the help of intravital microscopy, the availability of appropriate atherosclerotic animal models and first conclusive data obtained in humans, the important role of platelets in atheroprogression could be confirmed in vivo.
Conclusion: This review highlights the molecular machinery and inflammatory pathways used by platelets to initiate and accelerate atherothrombosis. Understanding the specific requirements for platelets adhering to endothelium may lead to the development of novel therapeutic strategies.