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Schematic illustration of the involvement of mitochondrial reactive oxygen species (ROS) in hypoxia-inducible factor 1 (HIF-1) stabilization. Mitochondrial ROS production has been shown to inhibit prolyl hydroxylase enzymes (PHDs) activity, thus preventing HIF-1α proteasomal degradation. Consequently, HIF-1α is stabilized and translocated to the nucleus, where it dimerizes with HIF-1β, initiating the transcription of HIF-1 responsiveness genes.
