Abstract
ObjectiveSepsis-induced myocardial dysfunction is a common complication of sepsis, characterized by high mortality and an unclear underlying mechanism. This study conducted an integrative multiomics analysis of mice with sepsis-induced myocardial dysfunction to provide new insights into potential mechanisms.MethodWe constructed an animal model of sepsis-induced myocardial dysfunction and analyzed the metabolomics, transcriptomics, and protein profiles of the heart tissues in the control and experimental groups.ResultsUntargeted metabolomics identified 74 significantly altered metabolites in the positive ion mode, of which 48 were upregulated and 26 downregulated; moreover, 70 significantly altered metabolites were detected in the negative ion mode, with 50 being upregulated and 20 downregulated. Transcriptomics revealed 4831 differentially expressed genes, with 3027 being downregulated and 1804 upregulated. Proteomics identified 107 significant proteins, 94 of which were significantly upregulated and 13 significantly downregulated. Integrated omics analysis revealed three significantly altered metabolites common to both groups: L-glutamate, L-aspartate, and nicotinamide. These metabolites were predominantly involved in nicotinate and nicotinamide metabolism, histidine metabolism, and nitrogen metabolism, potentially related to the pathogenesis of sepsis-induced myocardial dysfunction.ConclusionThe pathogenesis of sepsis-induced myocardial dysfunction in mice may be associated with alterations in nicotinate and nicotinamide metabolism, histidine metabolism, and nitrogen metabolism.