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This occurs through the PI3K/Akt pathway, which blocks FoxO-mediated transcription of these atrophy genes (Sacheck et al., 2004)

In the face of controversies and challenges, it is essential to establish a more efficient translational interface between science, technology, and clinical practice, driving mitochondrial metabolic reprogramming therapy from a potential pathway to clinical reality. Conclusion Mitochondrial metabolic reprogramming plays a central role in the therapeutic failure of CRC