Abstract
Mitochondria fulfill a number of essential cellular functions, being recognized that the strict regulation of the structure, function and turnover of these organelles is an immutable control node for the maintenance of neuronal integrity and homeostasis. Many lines of evidence posit that mitochondria constitute a convergence point of preconditioning - a paradigm that affords robust brain tolerance in the face of neurodegenerative insults. Indeed, it has been described that preconditioning activates an adaptive reprogramming of mitochondrial biology in response to a noxious stress-stimulus, which in turn will contribute to augment both mitochondrial and neuronal tolerance. Mitochondrial reactive species (ROS), mitochondrial ATP-sensitive potassium (mitoKATP) channels and mitochondrial permeability transition pore have been identified as specific mitochondrial mediators and targets of the adaptive program underlying preconditioning. Recent studies further link mitochondrial biogenesis, dynamics and mitophagy to preconditioning, thereby representing novel mechanisms by which preconditioning may mediate brain tolerance. The present review summarizes the current views on how mitochondrial biology is linked to preconditioning-induced neuroprotection. A better understanding of the mitochondrial mechanisms underlying preconditioning will help in the development of novel therapeutic approaches with the primary goal of modulating mitochondria to enhance brain tolerance against neurodegenerative events.
Keywords: Mitochondria, mitochondrial dynamics, mitochondria turnover, neuroprotection, preconditioning, reactive oxygen species, neurons, diazoxide, cytochrome c, mitophagy
Current Pharmaceutical Design
Title: New Insights into the Mechanisms of Mitochondrial Preconditioning-Triggered Neuroprotection
Volume: 17 Issue: 31
Author(s): Sonia C. Correia, Susana Cardoso, Renato X. Santos, Cristina Carvalho, Maria S. Santos, George Perry, Mark A. Smith and Paula I. Moreira
Affiliation:
Keywords: Mitochondria, mitochondrial dynamics, mitochondria turnover, neuroprotection, preconditioning, reactive oxygen species, neurons, diazoxide, cytochrome c, mitophagy
Abstract: Mitochondria fulfill a number of essential cellular functions, being recognized that the strict regulation of the structure, function and turnover of these organelles is an immutable control node for the maintenance of neuronal integrity and homeostasis. Many lines of evidence posit that mitochondria constitute a convergence point of preconditioning - a paradigm that affords robust brain tolerance in the face of neurodegenerative insults. Indeed, it has been described that preconditioning activates an adaptive reprogramming of mitochondrial biology in response to a noxious stress-stimulus, which in turn will contribute to augment both mitochondrial and neuronal tolerance. Mitochondrial reactive species (ROS), mitochondrial ATP-sensitive potassium (mitoKATP) channels and mitochondrial permeability transition pore have been identified as specific mitochondrial mediators and targets of the adaptive program underlying preconditioning. Recent studies further link mitochondrial biogenesis, dynamics and mitophagy to preconditioning, thereby representing novel mechanisms by which preconditioning may mediate brain tolerance. The present review summarizes the current views on how mitochondrial biology is linked to preconditioning-induced neuroprotection. A better understanding of the mitochondrial mechanisms underlying preconditioning will help in the development of novel therapeutic approaches with the primary goal of modulating mitochondria to enhance brain tolerance against neurodegenerative events.
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Cite this article as:
C. Correia Sonia, Cardoso Susana, X. Santos Renato, Carvalho Cristina, S. Santos Maria, Perry George, A. Smith Mark and I. Moreira Paula, New Insights into the Mechanisms of Mitochondrial Preconditioning-Triggered Neuroprotection, Current Pharmaceutical Design 2011; 17 (31) . https://dx.doi.org/10.2174/138161211798072490
DOI https://dx.doi.org/10.2174/138161211798072490 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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