Salvage of ischemic myocardium: a focus on JNK.
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.
Duplain
Hervé
H
Department of Internal Medicine and Botnar Center for Clinical Research, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. hduplain@hospvd.ch
D000818:Animals; D017209:Apoptosis; D016923:Cell Death; D002470:Cell Survival; D048670:MAP Kinase Kinase 4 / Q000502:physiology*; D020935:MAP Kinase Signaling System; D008954:Models, Biological; D009203:Myocardial Infarction / Q000473:pathology*; D017202:Myocardial Ischemia / Q000473:pathology / Q000628:therapy*; D015428:Myocardial Reperfusion Injury / Q000473:pathology; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D009336:Necrosis; D051381:Rats; D015427:Reperfusion Injury; D013997:Time Factors
D048670:MAP Kinase Kinase 4