Abstract
There is extensive evidence that the restoration of blood flow following cerebral ischemia contributes greatly to the pathophysiology of ischemia mediated brain injury. The initiating stimulus of reperfusion injury is believed to be the excessive production of reactive oxygen (ROS) and nitrogen (RNS) species by the mitochondria. ROS and RNS generation leads to mitochondrial protein, lipid and DNA oxidation which impedes normal mitochondrial physiology and initiates cellular death pathways. However not all ROS and RNS production is detrimental. It has been demonstrated that low levels of ROS production are protective and may serve as a trigger for activation of ischemic preconditioning. Ischemic preconditioning is a neuroprotective mechanism which is activated upon a brief sublethal ischemic exposure and is sufficient to provide protection against a subsequent lethal ischemic insult. Numerous proteins and signaling pathways have been implicated in the ischemic preconditioning neuroprotective response. In this review we examine the origin and mechanisms of ROS and RNS production following ischemic/reperfusion and the role of free radicals in modulating proteins associated with ischemic preconditioning neuroprotection.
Keywords: Epsilon PKC, HIF, Ischemic preconditioning, Nrf2, Reactive oxygen species, Sirtuin, SIRT1, Reperfusion
Current Neuropharmacology
Title:Redox Signaling Pathways Involved in Neuronal Ischemic Preconditioning
Volume: 10 Issue: 4
Author(s): John W. Thompson, Srinivasan V. Narayanan and Miguel A. Perez-Pinzon
Affiliation:
Keywords: Epsilon PKC, HIF, Ischemic preconditioning, Nrf2, Reactive oxygen species, Sirtuin, SIRT1, Reperfusion
Abstract: There is extensive evidence that the restoration of blood flow following cerebral ischemia contributes greatly to the pathophysiology of ischemia mediated brain injury. The initiating stimulus of reperfusion injury is believed to be the excessive production of reactive oxygen (ROS) and nitrogen (RNS) species by the mitochondria. ROS and RNS generation leads to mitochondrial protein, lipid and DNA oxidation which impedes normal mitochondrial physiology and initiates cellular death pathways. However not all ROS and RNS production is detrimental. It has been demonstrated that low levels of ROS production are protective and may serve as a trigger for activation of ischemic preconditioning. Ischemic preconditioning is a neuroprotective mechanism which is activated upon a brief sublethal ischemic exposure and is sufficient to provide protection against a subsequent lethal ischemic insult. Numerous proteins and signaling pathways have been implicated in the ischemic preconditioning neuroprotective response. In this review we examine the origin and mechanisms of ROS and RNS production following ischemic/reperfusion and the role of free radicals in modulating proteins associated with ischemic preconditioning neuroprotection.
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Cite this article as:
W. Thompson John, V. Narayanan Srinivasan and A. Perez-Pinzon Miguel, Redox Signaling Pathways Involved in Neuronal Ischemic Preconditioning, Current Neuropharmacology 2012; 10 (4) . https://dx.doi.org/10.2174/1570159X11209040354
DOI https://dx.doi.org/10.2174/1570159X11209040354 |
Print ISSN 1570-159X |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6190 |
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