Sepsis-induced myocardial dysfunction is associated with high mortality in sepsis. However, the underlying mechanisms of sepsis-induced myocardial dysfunction remain unclear. The heart is an energy-demanding organ. Under basal physiological conditions, cardiomyocytes rely primarily on energy provided by fatty acid oxidation. However, recent studies have revealed the important role of metabolic rearrangements in cardiomyocytes under some pathological conditions. 3-hydroxybutyrate dehydrogenase 1 (BDH1) is a key enzyme in ketone body metabolism, catalyzing the interconversion of acetoacetate and (R)-3-hydroxybutyrate. Previous studies have demonstrated the role of BDH1 in myocardial metabolic remodeling during acute fasting, but the expression patterns and functions of BDH1 in the septic heart are unknown. The aim of this study was to identify the interactors of BDH1 in H9C2 rat cardiomyocytes with or without lipopolysaccharide (LPS) treatment.