Fig. 2.

Mechanisms of plaque erosion. Endothelial cells of atherosclerotic plaques commonly express Toll-like receptor −2 (TLR2) that can ligate both Gram-positive toxins (G+ toxins) of bacterial pathogens and hyaluronan released from the extracellular matrix. TLR2 ligation can trigger endothelial dysfunction with endoplasmic reticulum stress and apoptosis. Such reactions are further enhanced by neutrophil attack on the endothelium. As a result, endothelial cells may detach, exposing the subendothelial matrix with its thrombogenic components. Activated neutrophils contribute to a prothrombotic state by releasing a set of proteases including neutrophil elastase and by forming neutrophil extracellular traps (NETs) that can damage endothelial cells, trap leucocytes and enhance thrombosis. PAD4, Peptide arginine deaminase-4, a component of NETs.