The aims of the present study were to determine: (1) the impact of aging on the myocardial inflammatory responses to sepsis in a cecal ligation and puncture model using old mice; (2) the effect of TLR2 knockout on the myocardial inflammatory responses in old septic mice; (3) the contribution of TLR2-mediated myocardial inflammatory responses to cardiac dysfunction and mortality caused by sepsis in old mice. This evidence concerns the gene TLR2 and Sepsis.