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 has suggested that mitochondrial (dys)function, ROS/RNS levels, and aberrations in mitochondrial morphology are interconnected, albeit in a cell- and context-dependent manner. In this Cell Metabolism Perspective paper Peter Willems (photo right) and Werner Koopman (photo left), Dept. of Biochemistry, theme Mitochondrial diseases in collaboration with Cindy Dieteren, Dept. of Cell Biology, Rodrigue Rossignol (Bordeaux, France) and Mike Murphy (Cambridge, UK), propose a mechanism in which ROS and RNS are involved in the short-term regulation of mitochondrial morphology and function. This control is exerted via non-transcriptional pathways by (local) action of ROS/RNS on mitochondrial fusion and fission proteins, allowing (auto)regulation of mitochondrial morphology and function by redox signals. Understanding this mechanism is crucial to unravel the pathological events in the many human disorders where redox homeostasis, mitochondrial function, and structure are disturbed, as well as to develop successful rational intervention strategies.
Peter H.G.M. Willems, Rodrigue Rossignol, R., Cindy E.J. Dieteren, Mike P. Murphy and Werner J.H. Koopman (2015) Redox homeostasis and mitochondrial dynamics. Cell Metab. (in press).
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