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- W2036697787 endingPage "600" @default.
- W2036697787 startingPage "579" @default.
- W2036697787 abstract "During cardiac ischemia-reperfusion (IR) injury, excessive generation of reactive oxygen species (ROS) and overload of Ca(2+) at the mitochondrial level both lead to opening of the mitochondrial permeability transition (PT) pore on reperfusion. This can result in the depletion of ATP, irreversible oxidation of proteins, lipids, and DNA within the cardiomyocyte, and can trigger cell-death pathways. In contrast, mitochondria are also implicated in the cardioprotective signaling processes of ischemic preconditioning (IPC), to prevent IR-related pathology. 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 direct effects of NO* on mitochondria are the focus of this review." @default.
- W2036697787 created "2016-06-24" @default.
- W2036697787 creator A5060599255 @default.
- W2036697787 creator A5064702019 @default.
- W2036697787 date "2008-03-01" @default.
- W2036697787 modified "2023-10-09" @default.
- W2036697787 title "Mitochondria as a Target for the Cardioprotective Effects of Nitric Oxide in Ischemia–Reperfusion Injury" @default.
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