Therefore, the present study demonstrates that ICA cell-derived NE is another factor in activating cardiomyocyte CaMKII via β1-AR to enhance LPS-induced cardiac inflammation, and β1-AR-CaMKII activation is the principal mechanism by which ICA cell-derived NE enhances cardiomyocyte NF-κB and MAPK signaling to promote LPS-induced cardiomyocyte TNF-α production. Here, NFKB1 is linked to inflammatory response.