The innate immune system is well recognized as the first line defense of foreign pathogens; however,
it can also recognize endogenous signals released from injured tissues and induce sterile inflammation. Toll-like
receptors (TLRs) and Nod-like receptors (NLRs) have been identified as its receptors, and they have been
shown to play a key role in the disease processes of sterile inflammation, including myocardial infarction (MI).
In particular, NLRs are the key components of the caspase-1 activating platform known as the “inflammasome,”
which produces the potent proinflammatory cytokine interleukin-1β. The current article reviews the role of the innate immune
system, especially TLRs and inflammasomes, in the pathophysiology of MI.