Figure 1. The endogenous metabolite N‐acetyl‐L‐tyrosine triggers mitohormesis in response to stress.

Mild perturbations of mitochondrial function, leading to an increase in mitochondria‐derived ROS, activate a retrograde mitochondria‐to‐nucleus signaling mechanism, which induces transcription of various genes involved in cellular stress response via redox‐sensitive transcription factors, e.g., FOXO (nematodal DAF‐16), NRF2 (nematodal SKN‐1), and HSF1, a process termed mitohormesis. Matsumura et al identify the endogenous metabolite N‐acetyl‐L‐tyrosine, which is formed in response to stress from its precursor tyrosine, as a triggering factor of mitohormesis in animal cells. mtUPR: mitochondrial unfolded protein response; ROS: reactive oxygen species. Modified from [Ref. 6].