CaMKII/calpain interaction mediates ischemia/reperfusion injury in isolated rat hearts.

Previous studies indicated that Ca/calmodulin-dependent kinase II (CaMKII), a kinase involved in the modulation of ryanodine receptor activity, activates Ca-regulated protease μ-calpain to promote myocardial ischemia/reperfusion injury. This study was performed to explore the underlying mechanisms in CaMKII-induced calpain activation to better understand heart injury. To examine the Ca paradox and ischemia/reperfusion injury, isolated rat hearts were subjected to a Ca-free solution for 3 min, or left coronary artery occlusion for 40 min, prior to restoration of normal perfusion.