NR4A1 and myocardial infarction: NR4A1 was also found to contribute to limit the influx of inflammatory monocytes and the production of inflammatory cytokines during myocardial infarction and NR4A1-dependent Ly6Clow monocytes have demonstrated a crucial role in mediating intravascular homeostasis by regulating necrosis of endothelial cells [4, 5].