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Because mtDNA depletion or OXPHOS impairment profoundly alters redox state, membrane potential, ATP production, and metabolite distribution between mitochondria and cytosol [80], mitochondrial dysfunction can act as a source of epigenetic perturbation interventions that selectively inhibit OXPHOS complexes or mitochondrial carrier transporters can therefore help define the molecular identity of these mitochondria-derived epigenetic cues

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We found that high M1 level was associated with advanced grade (Fig