NLRP3 and Atherosclerotic lesion: MARK4 participates in the high glucose-induced NLRP3 inflammasome activation, thus mediating IL-1β and IL-18 expression in vascular endothelial cells [23]; in addition, MARK4 deficiency inhibited hypoxia/reoxygenation (H/R)-induced NLRP3 inflammasome activation [39]; moreover, positive MARK4 expression has been observed in human atherosclerotic lesions, and MARK4 deficiency in BMDMs reduced cholesterol crystal-induced NLRP3 inflammasome activation [16].