This figure depicts a plaque in a carotid artery bifurcation on top. Intraplaque hemorrhage can arise because of rupture of the fibrous, a breach in endothelial integrity, or disruption of the barrier function and leakage from plaque microvessels. Erythrocytes lyse readily in the plaque microenvironment, releasing iron and its prosthetic heme group. The heme-derived redox-active iron can drive oxidative stress through the Fenton reaction by generating hydroxyl radical (•OH). Iron can enter smooth muscle cells (not shown) and macrophages or smooth muscle cells by erythrophagocytosis. The phagocytes exposed to red blood cells and their products elaborate biliverdin reductase and heme oxygenase, enzymes involved in the catabolism of the heme moiety. The concentrations of these enzymes in plasma may be associated with cardiovascular risk. The phagocytes that have engulfed erythrocytes and their products can modulate inflammation both positively and negatively, with an uncertain net effect.