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Cell Metab. 2015 Aug 4;22(2):207-18. doi: 10.1016/j.cmet.2015.06.006. Epub 2015 Jul 9.

Redox Homeostasis and Mitochondrial Dynamics.

Author information

1
Department of Biochemistry, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, 6500HB Nijmegen, The Netherlands.
2
University of Bordeaux, Maladies Rares: Génétique et Métabolisme (MRGM), 330000 Bordeaux, France.
3
Department of Cell Biology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, 6500HB Nijmegen, The Netherlands.
4
MRC Mitochondrial Biology Unit, Wellcome Trust/MRC Building, Cambridge CB2 0XY, UK.
5
Department of Biochemistry, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, 6500HB Nijmegen, The Netherlands. Electronic address: werner.koopman@radboudumc.nl.

Abstract

Within living cells, mitochondria are considered relevant sources of reactive oxygen species (ROS) and are exposed to reactive nitrogen species (RNS). During the last decade, accumulating evidence suggests that mitochondrial (dys)function, ROS/RNS levels, and aberrations in mitochondrial morphology are interconnected, albeit in a cell- and context-dependent manner. Here it is hypothesized that ROS and RNS are involved in the short-term regulation of mitochondrial morphology and function via non-transcriptional pathways. We review the evidence for such a mechanism and propose that it allows homeostatic control of mitochondrial function and morphology by redox signaling.

PMID:
26166745
DOI:
10.1016/j.cmet.2015.06.006
[Indexed for MEDLINE]
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