Megakaryocytes from them , and the resultant platelet synthesize many pro-inflammatory and pro - atherosclerotic lesions. These mediators are stored in a platelet granules . Platelet activation induces the release of mediators in the extracellular environment . Resting platelets do not adhere to unstimulated endothelial cells and do not react with them and with the vessel wall . Activation of endothelial cells and / or platelets triggers the inflammation, which causes inter alia atherosclerosis . This article describes the mechanisms that are responsible for initiating the formation of inflammatory foci , involving activated platelets and endothelial cells . The activation of platelets and endothelium participates are many mediators released by the likes platelets , endothelial cells , leukocytes , smooth muscle cells , and microvesicles derived from blood cells and endothelial cells. The mediators contribute to the propagation of fire. Inflammatory mediators acting in an autocrine and paracrine manner , activation of platelets and heighten endothelial inflammation area increase , accelerating deposition of lipid lesions in atherosclerosis and increase deposits . This article describes the construction and operation of some mediators released from platelets , which are inflammatory markers . Also described are the signaling pathways activated by proinflammatory mediators in endothelial cells . The signal transduction involves a variety of kinases and adapter proteins which , depending on the operating mediator , lead to an increase in the activity of various nuclear factors , responsible for increased protein synthesis of pro-inflammatory and pro - atherosclerotic lesions.