Activation of macrophage inflammasomes leads to interleukin (IL)-1β and IL-18 secretion
and promotes atherosclerosis and its complications in mice and humans. However, the
specific role and underlying mechanisms of the inflammasome in atherogenesis are topics
of active research. Several studies in hyperlipidemic mouse models found that the NOD-like
receptor protein 3 (NLRP3) inflammasome contributes to atherosclerosis, but recent work
suggests that a second hit, such as defective cholesterol efflux or accumulation of oxidized …