Figure 2.

Potential roles of MPO and MPO-derived oxidants in promoting atherosclerotic plaque instability. MPO can affect a number of processes that contribute to plaque instability and possible plaque rupture. MPO released by monocyte/macrophages and neutrophil can activate MMPs and inhibit TIMPs, leading to reduction in ECM, especially in the fibrous cap. In addition, MPO may contribute to a thrombogenic environment by inducing endothelial cells to release tissue factor and by priming of platelet aggregation. Finally, MPO can increase endothelial cell (EC) permeability and apoptosis, thereby increasing the leakiness of the endothelium.