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Beyond direct transplantation, nanotechnologies, such as the MITO-Porter liposomal system, offer a means of targeted mitochondrial delivery, fusing with mitochondrial membranes to restore function, and have shown promise in doxorubicin-induced cardiomyopathy models [1, 240]

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42 AKT directly and indirectlyby the activation of mTOR, which promotes the stabilization of the transcription factor hypoxia-inducible factor-1stimulates the expression of glucose transporters and key glycolytic enzymes (Figure 3)