Role of NLRP3 Inflammasome in Cardiac Inflammation and Remodeling after Myocardial Infarction

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An accumulating body of evidence indicates that inflammation plays a crucial role in the pathophysiology of myocardial infarction (MI). Nucleotide-binding oligomerization domain-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome is an intracellular multiprotein complex that regulates caspase-1 activation and the subsequent processing of the potent inflammatory cytokine interleukin (IL)-1β as well as triggering inflammatory cell death pyroptosis. We and other investigators demonstrated that deficiency of the NLRP3 inflammasome components reduces inflammation and improves cardiac dysfunction and remodeling in rodent models of MI. Therefore, the regulation of NLRP3 inflammasome has been regarded as a potential therapeutic target for MI. Furthermore, a recent Canakinumab Antiinflammatory Thrombosis Outcome Study (CANTOS) trial revealed the efficacy of IL-1β inhibition in preventing recurrent cardiovascular events in patients with MI. This review focuses on the role of NLRP3 inflammasome in the process of cardiac inflammation and remodeling after MI, and discusses its potential as a therapeutic target for the prevention and treatment of MI.