To the best of our knowledge, the present study presents for the first time the direct evidence that cardiomyocyte β1-AR activation plays a pivotal role in cardiomyocyte apoptosis during endotoxemia, and cardiomyocyte β1-AR activation promotes LPS-induced cardiomyocyte apoptosis through activating PKA, increasing cytosolic Ca2+ concentration and CaMKII activation as well as enhancing IκBα phosphorylation and TNF-α expression in cardiomyocytes (Figure 9). Here, CAMK2G is linked to serum lipopolysaccharide activity.