Invited Review ArticleCell-Specific Roles of NLRP3 Inflammasome in Myocardial InfarctionTakahashi, Masafumi MD, PhDAuthor Information Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan. Reprints: Masafumi Takahashi, MD, PhD, Division of Inflammation Research Center for Molecular Medicine, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan (e-mail: [email protected]). The author reports no conflicts of interest. Journal of Cardiovascular Pharmacology: September 2019 - Volume 74 - Issue 3 - p 188-193 doi: 10.1097/FJC.0000000000000709 Buy Metrics Abstract An accumulating body of evidence indicates that NLRP3 inflammasome plays a crucial role in the pathophysiology of cardiovascular diseases, including atherosclerosis and acute myocardial infarction (MI). NLRP3 inflammasome is a multimeric protein complex that leads to activation of caspase-1, which further induces maturation of interleukin (IL)-1β and IL-18. Activated caspase-1 also induces a particular form of cell death called pyroptosis by the cleavage of gasdermin D. Our and other groups have shown that inhibition of the NLRP3 inflammasome attenuates the inflammatory response and ameliorates myocardial dysfunction and remodeling in animal models of acute MI. Interestingly, investigations have suggested that NLRP3 inflammasome has cell-specific roles in different cell types, such as inflammatory cells, cardiomyocytes, cardiac fibroblasts, and vascular endothelial cells, after acute MI. Moreover, the recent CANTOS trial showed that inhibition of IL-1β was efficacious in secondary prevention for cardiovascular events in patients with previous MI. These findings suggest that NLRP3 inflammasome may be a potential target for the prevention and therapy of MI. This review summarizes recent knowledge on NLRP3 inflammasome and focuses on its cell-specific roles in acute MI. Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.