Abstract: NLRP3 inflammasome is an intracellular multiprotein complex that is the key mediator of aseptic inflammatory response and plays an important role in the pathophysiological mechanism of myocardial infarction (MI). NLRP3 inflammasome regulates the activation of cysteine protease (caspase-1), promotes the production of inflammatory factors such as IL-1β, and is involved in programmed cell death. A large number of studies have shown that inhibiting NLRP3 inflammasome can effectively reduce the inflammatory response and improve cardiac dysfunction and remodeling after MI. Therefore, NLRP3 inflammasome may be a new therapeutic target to reduce the incidence of cardiovascular events and improve the prognosis. This article reviews the role of NLRP3 inflammasome in cardiac remodeling after MI.