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Background and Hypothesis: Pancreatic β-cells exhibit high levels of metabolic activity which generates reactive oxygen species (ROS). ROS can lead to β-cell damage and death, which could contribute to diabetes development. Therefore, pathways reducing ROS are of interest as potential therapeutic targets. We have demonstrated that IL-6 stimulates autophagy and protects β-cells from ROS and apoptosis. IL-6 also stimulates the translocation of NRF2 to the mitochondria, which is accompanied by several markers of mitophagy, the autophagic degradation of mitochondria. In this study, we ask where NRF2 fits in the pathway downstream of IL-6 by asking if NRF2 is required for IL-6 stimulation of autophagy and/or mitophagy.

IL-6 Stimulates Autophagy in Wild Type and NRF2 Knock Out Mice β-cells