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Salvage of ischemic myocardium: a focus on JNK
Advances in Experimental Medicine and Biology
Myocardial infarction is a problem of utmost clinical significance, associated with an important morbidity and mortality. Actual treatment of this affection is focusing on the reperfusion of the occluded coronary-artery. A complementary approach would be to prevent the death of the ischemic myocardium by interacting with detrimental intracellular pathways. Several strategies have been successfully used to reduce the size of myocardial infarction in animal models. In this article, we will focus on the c-Jun N-terminal kinase (JNK), a member of the mitogen-activated (MAPK) protein kinase family and an important determinant of cell survival/death. We will review the role of JNK in cardiac ischemia/reperfusion and summarize recent advances in the use of JNK inhibitors to protect the myocardium.
Animals Apoptosis Cell Death Cell Survival MAP Kinase Kinase 4/*physiology MAP Kinase Signaling System Models, Biological Myocardial Infarction/*pathology Myocardial Ischemia/pathology/*therapy Myocardial Reperfusion Injury/pathology Myocardium/*enzymology/pathology Necrosis Rats Reperfusion Injury Time Factors
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