Figure 9.

Participation of RBCs to atherothrombosis. Following plaque rupture, RBCs can further infiltrate the plaque where they are either phagocytosed (*) by endothelial cells, macrophages and vascular smooth muscle cells (VSMC), or lysed. Erythrocytes, by their adhesive and aggregation properties, exacerbated when glycated, also contribute, with platelets, to the thrombus formation. When glycated or aged, phosphatidylserine exposing erythrocytes can further interact with activated platelets [182]. This process participates in the occlusive phenomenon.