Molecular mechanism of myocardial injury due to ischemia-reperfusion.
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概要
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We review on the involvement of intracellular signaling molecules in the protection against myocardial ischemia-reperfusion injury. Ischemia or repeated brief ischemia-reperfusion (ischemic preconditioning, IP) induces translocation of PKC isoforms to the membrane or nucleus. PKC-ε isoform is involved in the IP's protective effect in the perfused heart and in vivo infarction model. In the in vivo model, IP upregulates VEGF mRNA and subsequent angiogenesis. Additionally, NO generated during reperfusion activates PKC-α, δ and ε isoforms, thereby alleviating contractile dysfunction by reperfusion. On the other hand, ischemia induces PKC-ζ translocation through PI3 kinase activation. Ischemia also induces MAP kinase, c-Jun-N-terminal kinase (JNK) to the nucleus, and reperfusion activates MAP kinase and JNK, thereby inducing c-fos and c-jun. The pathway of PI3 kinase, PKC-ζ, and MAP kinase protects myocardial cells against ischemia-reperfusion injury through apoptosis inhibition. Ischemia also induces translocation of small heat shock proteins HSP27 and MKBP to the nucleus and myofibrils, which would protect myofibrils and nucleus against oxidative stress induced by reperfusion.
- 日本電気泳動学会の論文
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