Abstract
Several years ago it was proposed that the AMP-activated protein kinase cascade might protect cells against stresses that deplete cellular ATP. Young et al. have now directly tested this by studying the effects of ischemia and reperfusion in perfused hearts from mice expressing a dominant-negative mutant that suppresses the kinase activity in cardiac muscle. Compared with control hearts, the mutant hearts showed clear evidence for increased necrotic damage and increased apoptosis. These findings may have implications for the treatment of ischemic heart disease.
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