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Abstract Septic cardiomyopathy (SCM) is an acute cardiac dysfunction involving myocardial cell pyroptosis. TREM‐1 is a known receptor on cell membrane that can amplify the inflammatory response. Our previous studies have shown that TREM‐1 in cardiomyocytes is involved in the activation of NLRP3 through the SMC4/NEMO pathway. Here, we aimed to use Trem‐1 and Nlrp3 knockout mice to verify the effect of TREM‐1 through NLRP3 on cardiac function in septic mice. The results showed that TREM‐1 knockout resulted in a decrease in the release of downstream cell signals, including SMC4 and NLRP3, resulting in a decrease in cytokine release and improvement of cardiac dysfunction. Knockout of NLRP3 also reduced cardiomyocyte pyroptosis and increased survival rate. The therapeutic targeting of TREM‐1 activation of NLRP3 and its pathway may contribute to the treatment or prevention of SCM.
Chen et al. (Mon,) studied this question.