Redox regulation of mitochondrial biogenesis.

Redox regulation of mitochondrial biogenesis.
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DOI:
10.1016/j.freeradbiomed.2012.09.014
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发表时间:
2012-12-01
影响因子:
7.4
通讯作者:
Suliman, Hagir B.
Suliman, Hagir B.
中科院分区:
医学1区
文献类型:
--
作者:
Piantadosi, Claude A.;Suliman, Hagir B.

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The cell renews, adapts, or expands its mitochondrial population during episodes of cell damage or periods of intensified energy demand by the induction of mitochondrial biogenesis. This bi-genomic program is modulated by redox-sensitive signals that respond to physiological nitric oxide (NO), carbon monoxide (CO), and mitochondrial reactive oxygen species (ROS) production. This review summarizes our current ideas about the pathways involved in the activation of mitochondrial biogenesis by the physiological gases leading to changes in the redox milieu of the cell with an emphasis on the responses to oxidative stress and inflammation. The cell’s energy supply is protected from conditions that damage mitochondria by an inducible transcriptional program of mitochondrial biogenesis that operates in large part through redox signals involving the nitric oxide synthase and the heme oxygenase-1/CO systems. These redox events stimulate the coordinated activities of several multifunctional transcription factors and co-activators also involved in the elimination of defective mitochondria and the expression of counter-inflammatory and anti-oxidant genes, such as IL10 and Sod2, as part of a unified damage-control network. The redox-regulated mechanisms of mitochondrial biogenesis schematically outlined in the graphical abstract link mitochondrial quality control to an enhanced capacity to support the cell’s metabolic needs while improving its resistance to metabolic failure and avoidance of cell death during periods of oxidative stress.
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