Redox Homeostasis and Mitochondrial Dynamics

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. Willems et al. explore the links between cellular and mitochondrial redox homeostasis and the non-transcriptional regulation of mitochondrial fission and fusion. Proper understanding of this rheostatic system is crucial to unravel how disturbed redox homeostasis, mitochondrial function, and mitochondrial structure are linked to pathology in human disorders.