The restoration of blood flow to the ischemic heart has often caused myocardial ischemic/reperfusion (MI/R) injury. An inflammatory response triggered by MI/R injury can irreversibly cause damage to the viable tissue surrounding the infarct, thereby further extending the injury. It is still unclear how innate immune signaling pathways are initiated during MI/R injury (43) . However, TLR4, which is also present in cardiomyocytes, has been thought to play a role in mediating MI/R injury. Schuster and Nelson (28) have shown that TLR4 receptor is up-regulated in response to myocardial injury. Furthermore, Shimamoto and colleagues have shown that TLR4 activates NF-κB-dependent transcription of inflammatory cytokine genes in MI/R injury. The TLR4-mediated injury appears to occur through activation of c-Jun NH 2terminal kinase (JNK) and translocation of NF-κB (41) . It is also believed that TLR4 recognizes endogenous molecules that are exposed during cellular injury and extracellular matrix remodeling, independent of pathogen invasion (44) . Thus, inhibition of TLR4 signaling pathway may be a potential therapeutic target to treat the myocardium damage in the ischemia/reperfusion setting.