Fig. 1.

Pathogenetic mechanisms linking erythrocyte oxidative modifications to thrombosis. Erythrocytes produce high quantities of intracellular reactive oxygen species (ROS), mostly by NADPH oxidase activation and haemoglobin autoxidation; furthermore, extracellular ROS released by other cells in the blood flow can be uptaken and accumulate within erythrocytes. This oxidative milieu can alter erythrocyte membrane, leading to an impaired erythrocyte function and promoting erythrocytes lysis, binding to endothelial cells (EC), activation of platelet, coagulation factors and leucocytes. Moreover, structurally altered erythrocytes are able to adhere to the vessel wall, contributing to thrombin generation within thrombus. This process results in an accelerated haemolysis and in a hypercoagulable state, in which structurally impaired erythrocytes contribute to increase thrombus size and to reduce its permeability and susceptibility to lysis. EC, endothelial cells; RBC, red blood cells; ROS, reactive oxygen species; SMC, smooth muscle cells.