Fig. 3

Microvasculature is a critical target of platelet activation in sepsis. Platelets circulate more concentrated close to the vascular wall and sense endothelium disturbances. In sepsis, many cellular and soluble actors concur to activate the endothelium. Activated/injured endothelium is a key driver of platelet activation. Signals generated by infection, inflammation and coagulation can also activate platelets in sepsis. The relative importance of platelet activation by PAMPs in sepsis is not well established. Platelet activation contributes to fuel various pro-inflammatory and pro-coagulant pathways with potential deleterious consequences on endothelium homoeostasis and integrity. Unmitigated platelet activation in sepsis may take a significant part in the complex global scenario that leads to impairment of the endothelium barrier and microcirculatory failure, a leading cause of organ dysfunction in sepsis. Only some pathophysiological events are schematized (see text for details). Scales are arbitrary. ROS reactive oxygen species, EC endothelial cells, NET neutrophils extracellular traps, PMPs platelet microparticles, ECM extracellular matrix