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. Author manuscript; available in PMC: 2015 May 6.
Published in final edited form as: Cell Metab. 2014 Feb 20;19(5):757–766. doi: 10.1016/j.cmet.2014.01.011

Figure 1.

Figure 1

The basis of mitohormesis. Any of a number of endogenous or exogenous stresses can perturb mitochondrial function. These perturbations are relayed to the cytosol through at present, poorly understood mechanisms that may involve mitochondrial ROS as well as other mediators. These cytoplasmic signaling pathways and subsequent nuclear transcriptional changes induce various long lasting cytoprotective pathways. This augmented stress resistance allows for protection from a wide array of subsequent stresses.