Employing an array of genetically modified murine models, including Dusp1 knockout (Dusp1cko), Dusp1 transgenic (Dusp1Tg), and Pgam1 knockout (Pgam1cko), our study sought to elucidate the consequences of dysregulated Pgam1, post-transcriptional dephosphorylation of Dusp1, and impaired MQC on myocardial function in the context of LPS-induced endotoxemia. This evidence concerns the gene PGAM1 and serum lipopolysaccharide activity.