Nrf2 is known to induce the expression of hundreds of cytoprotective proteins to counteract endogenously or exogenously generated oxidative stress when the body was stimulated by electrophilic reagents or reactive oxygen species. Interestingly

increasing evidence shows that Nrf2 is associated with mitochondrial biogenesis during environmental stresses in certain tissues such as the heart. Furthermore

Nrf2 activation was recently observed in the heart of surfeit locus protein 1（Surf1）-/-mice in which cellular respiration was decreased due to cytochrome c oxidase defects. In this review

we critically examine the relationship between Nrf2 and mitochondria

and argue that the Nrf2 stress pathway intimately communicates with mitochondria to maintain cellular homeostasis during oxidative stress.