FIGURE 7.

A schematic model of the function of melatonin in KD‐related vasculitis. KD‐related vasculitis is a crosstalk between vascular endothelial cells and immune cells, especially macrophages. Macrophages release pro‐inflammatory cytokines (such as IL‐6) to mediate damage to the vascular endothelial cells, and the damaged vascular endothelial cells in turn release more damage‐associated molecular patterns (DAMPs), to promote the secretion of pro‐inflammatory cytokines from the macrophages. Melatonin alleviates vascular endothelial cell injury directly, by suppressing apoptosis in an autophagy‐dependent manner, and also decreases the production of the pro‐inflammatory cytokines released by macrophages, thereby reducing the immunopathological damage of vascular endothelial cells in KD‐related vasculitis. ATG3, autophagy‐related gene‐3; CREB, cAMP response element‐binding protein; DAMP, damage‐associated molecular pattern; KD, Kawasaki disease; MT1, melatonin receptor 1; MT2, melatonin receptor 2