Role of the Inflammasome in Myocardial Infarction

Inflammation plays a crucial role in the pathophysiology of myocardial infarction (MI). In particular, reperfusion caused by increased thrombolytic activity or revascularization therapy may restore the coronary blood flow and reduce the infarct size, but it also simultaneously enhances the inflammatory response and causes harmful effects on the myocardium—a process termed ischemia-reperfusion (I/R) injury. The inflammasome is a large multiprotein complex that is formed in the cytosol in response to danger signals; it drives the proinflammatory cytokine interleukin (IL)-1β. Increasing evidence indicates that the inflammasome is a key player in the disease processes of sterile inflammation. In particular, IL-1β is a prominent and early mediator of inflammation in I/R injury, suggesting the importance of the inflammasome in myocardial I/R injury. This article reviews the role of the inflammasome in the development of myocardial I/R injury and discusses the potential of the inflammasome as a novel therapeutic target for the treatment of myocardial I/R injury.