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Sepsis is a systemic inflammatory response syndrome caused by a variety of dysregulated responses to host infection with life-threatening multi-organ dysfunction. Among the injuries or dysfunctions involved in the course of sepsis, cardiac injury and dysfunction often occur and are associated with the pathogenesis of hemodynamic disturbances, also defined as sepsis-induced cardiomyopathy (SIC). The process of myocardial metabolism is tightly regulated and adapts to various cardiac output demands. The heart is a metabolically flexible organ capable of utilizing all classes of energy substrates, including carbohydrates, lipids, amino acids, and ketone bodies, to produce ATP. The demand of cardiac cells for energy metabolism changes substantially in septic cardiomyopathy, with distinct etiological causes and different times. This review describes changes in cardiomyocyte energy metabolism under normal physiological conditions and some features of myocardial energy metabolism in septic cardiomyopathy and briefly outlines the role of the mitochondria as a center of energy metabolism in the septic myocardium, revealing that changes in energy metabolism can serve as a potential future therapy for infectious cardiomyopathy., Competing Interests: Declaration of competing interest The authors do not have relevant conflicts of interest to disclose., (Copyright © 2024 Hellenic Society of Cardiology. Publishing services by Elsevier Inc. All rights reserved.)

Background: tRNA-derived small RNAs (tsRNAs) as a novel non-coding RNA have been studied in many cardiovascular diseases, but the relationship between tsRNAs and septic cardiomyopathy has not been investigated. We sought to analyze changes of the expression profile of tsRNAs in septic cardiomyopathy and reveal an important role for tsRNAs. Methods: We constructed a sepsis model by cecal ligation and puncture (CLP) in mice, and microarray analysis was used to find differentially expressed tsRNAs. Quantitative real-time PCR was used to verify the expression of tsRNAs and the interference effect of angiogenin (ANG), a key nuclease producing tsRNAs. Bioinformatics analysis was used to predict target genes and functions. CCK-8 and LDH release assays were used to detect cell viability and cell death. Results: A total of 158 tsRNAs were screened, of which 101 were up-regulated and 57 were down-regulated. A total of 8 tsRNAs were verified by qPCR, which was consistent with microarray results. Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses suggest that these tsRNAs may be associated with the Wnt signaling pathway and participate in cellular process. The expression of tsRNAs decreased after the interference of the key nuclease ANG, while CCK-8 suggested a corresponding decrease in cell viability and an increase in the release of LDH (cell death), indicating that tsRNAs can protect cardiomyocytes during the development of septic cardiomyopathy, reduced cardiomyocyte death. Conclusions : A total of 158 tsRNAs changed significantly in septic cardiomyopathy, and these tsRNAs may play a protective role in the development of septic cardiomyopathy.