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Once synthesized, MOTS-c is actively transported out of the mitochondria and into the nucleus during conditions like exercise or metabolic stress

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Replicative endothelial cell senescence may lead to endothelial dysfunction by increasing the BH2/BH4 ratio induced by oxidative stress, reducing BH4 availability, and decreasing the expression of eNOS

GPx7 likes to interact with the domain of PDI, and intramolecular cooperation between the two redox-active sites of PDI increases the activity of the Ero1/GPx7/PDI triplet, thereby promoting protein folding mechanisms (Wang et al., 2014) (Figure 6)