Myocardial infarction (MI) is the most severe manifestation of coronary artery disease which may lead to heart failure. One of the crucial mechanisms causing MI induced complications is inflammasome activation and subsequent release of inflammatory cytokines. A significant rise in troponin I, creatine kinase-MB (CK-MB), interleukin 1β (IL-1β) serum levels and nuclear factor-kappa B (NF-κB) were observed in MI. Moreover, increase in the expression of all inflammasome components was detected

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... with histopathological and electrocardiographic abnormalities. The current mini-review shows that targeting the inflammatory cascade through inflammasome inhibition may be a novel strategy for management of MI and preventing its complications.