Stressed Out: Mitohormesis Is Crossing Borders

Labbadia et al. showed that low-dose mitochondrial stress promotes protein homeostasis in the cytosol to endure proteotoxic conditions, particularly during aging. This hormetic mitochondrial stress response is heat shock factor 1 (HSF1)-dependent and, remarkably, does not affect physiological parameters that are usually associated with pathogenic disturbance of mitochondrial function.