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. 2021 Jun 7;12:637598. doi: 10.3389/fimmu.2021.637598

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Copyright © 2021 Zhou, Li, Chen, Huang, Qin and Li.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic of the role of TUG1 in CME-induced myocardial injury. Once CME occurs, the expression of lncRNA TUG1 in cardiomyocytes is inhibited. The TUG1 level in the cytoplasm of cardiomyocytes significantly decreases, and the competitive adsorption of miR-186-5p weakens accordingly, which leads to the increase of miR-186-5p level. The increased miR-186-5p directly binds to the 3' UTR of XIAP mRNA and promotes its degradation, resulting in a significant decrease in XIAP expression. The decrease in XIAP leads to an increase in NLRP3 inflammasomes (composed of NLRP3, ASC, caspase-1 protein) and promotes pyroptosis, which ultimately further aggravates CME-induced myocardial injury. Breaking this TUG1/ miR-186-5p/XIAP/NLRP3 inflammasome-mediated pyroptosis pathway may be a new therapeutic target for CME-induced myocardial injury.