Fig. 4
From: Neutrophil extracellular traps in acute coronary syndrome
Schematic illustration of the molecular mechanisms of neutrophil extracellular traps (NETs) in myocardial infarction (MI). Cardiac myocyte necrosis in the inflammatory site, HDC and PRMTI act as upstream regulatory signals and directly stimulate neutrophils and promote NETs expression. Additionally, PAD4 and APOE regulate the polarisation of macrophages, indirectly activating neutrophils and promoting the expression of NETs. Furthermore, NETs and inflammatory cells work together on myocardial cells, which damage myocardial cells and induce MI through continuous processes of inflammatory reaction, myocardial cell necrosis and scar formation