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KMID : 0880520100460030129
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Chonnam Medical Journal
2010 Volume.46 No. 3 p.129 ~ p.139
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Mechanism of Ischemia and Reperfusion Injury to the Heart: From the Viewpoint of Nitric Oxide and Mitochondria
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Han Sang-Jin
Kim Weon
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Abstract
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After an acute myocardial infarction, early and successful myocardial reperfusion is the most effective strategy for reducing the size of a myocardial infarct and improving the clinical outcome. However, the process of restoring blood flow to the ischemic myocardium can induce injury. This phenomenon,termed myocardial reperfusion injury, can paradoxically reduce the beneficial effects of myocardial reperfusion and lead to lethal damage to myocardium. During cardiac ischemia-reperfusion (IR) injury, excessive generation of reactive oxygen species (ROS), overload of intracellular Ca2+, H+ leakage at the mitochondrial level, inflammation, and metabolic modulations lead to opening of the mitochondrial permeability transition pore(PTP) on reperfusion. This can result in the depletion of ATP, irreversible oxidation of proteins, lipids, and DNA within the cardiomyocyte, and can trigger apoptosis. In contrast, mitochondria also plays an important role in the cardioprotective signaling processes of ischemic preconditioning (IPC), to prevent IR injury. Nitric oxide (NO) generated constitutively within the heart has long been known to influence myocardial function. But, Nitric oxide (NO) has emerged as a potent effector molecule for a variety of cardioprotective strategies, including IPC. Whereas NO is most noted for its activation of the "classic" soluble guanylate cyclase (sGC) signaling pathway, emerging evidence indicates that NO can directly act on mitochondria, independent of the sGC pathway, affording acute cardioprotection against IR injury. These effects of NO on mitochondria and mitochondrial role during IR injury are the focus of this review.
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KEYWORD
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Myocardial infarction, Ischemia-reperfusion, Nitric oxide, Mitochondria
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