AbstractAdriamycin (ADR) is a widely used chemotherapeutic agent. However, dose-related cardiomyopathy that may lead to
congestive heart failure is a major limiting factor for the clinical application of ADR. The most prevailing hypothesis for ADR-induced cardiac injury is the increases of oxidative stress. The previous study in our laboratory has demonstrated that overexpression of MnSOD in the transgenic mice protected against ADR-induced acute cardiac injury. Tumor necrosis factor-α (TNF-α), a pro-inflammatory cytokine produced also by
cardiomyocytes, is a well-known MnSOD inducing factor with both adaptive and maladaptive effects on
cardiac function. In the present study, we…
