The Effects Of C-Jun N-terminal Kinase After Myocardial Ischemia And Reperfusion In Anaesthetized Rats

Apoptosis is an active gene-directed cell death process which plays a key role in myocardial reperfusion injury. Cardiac myocyte cell death triggered by ischemia/ reperfusion can occur by both apoptosis and necrosis. While cell death after prolonged periods of ischemia is ascribed to necrosis, apoptosis occurs in cells and tissues exposed to reoxygenation after ischemia. The intracellular signaling pathways that mediate stress responses of cardiomyocytes are not fully delineated. However, it has recently been demonstrated that myocardial ischemia/reperfusion activates the two 'stress-responsive' mitogen-activated protein kinase (MAPK) subfamilies, namely, c-Jun N-terminal kinases (JNK) and p38 mitogen-activated protein kinases (p38-MAPKs), resulting in apoptosis. While p38-MAPK is activated by ischemia and this activation state is maintained during reperfusion, activation of JNK occurs only during reperfusion. Therefore, inhibition of apoptosis could be a therapeutic approach for reducing myocardial damage after oxidative stress.