To elucidate the pathophysiological consequences of Dusp1 downregulation in endotoxemia-induced myocardial dysfunction, we engineered cardiomyocyte-specific Dusp1 knockout (Dusp1cko) mice and established a lipopolysaccharide (LPS)-induced endotoxemia myocardial model. This evidence concerns the gene DUSP1 and serum lipopolysaccharide activity.