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The image provided on the cover page depicts small roundworms named C. elegans that have been loaded with a fluorophore to allow quantification of mitochondrial production of reactive oxygen species (ROS). Schmeisser et al. studied the influence of a compound-based inhibition of mitochondrial complex I on stress resistance, physical activity and life expectancy in C. elegans that were shown to be improved upon compound-based inhibition. Similar to dietary restriction (DR), compound-based inhibition of mitochondrial complex I caused intracellular energy deprivation and increase production of ROS. However, only the latter was responsible for the observed beneficial outcomes. While known energy sensors such as AMPK or sirtuins were not involved, lifespan extension was dependent on transiently increased ROS formation in redox-sensitive neurons and the p38/NRF-2 redox-signaling cascade. Interestingly, complex I inhibition does not further extend the lifespan of nematodes exposed to DR, suggesting that both interventions share a common denominator that is unexpectedly not energy deprivation but neuronal ROS signaling.

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The 60 Second Metabolist
In this section authors briefly report on their work recently published in Molecular Metabolism.

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Amna Khamis
University of Lille, CNRS, Institute Pasteur de Lille, Lille, France
Referring article

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