Abstract
Axon regeneration requires a substantial mitochondrial energy supply. However, injured mature neurons often fail to regenerate due to their inability to meet these elevated energy demands. Our findings indicate that harmine compensates for the energy deficit following axonal injury by enhancing the coupling between glucose metabolism and mitochondrial homeostasis, thereby promoting axon regeneration. Notably, harmine facilitates mitochondrial biogenesis and enhances mitophagy, ensuring efficient mitochondrial turnover, and energy supply. Thus, harmine plays a crucial role in enhancing glucose metabolism to maintain mitochondrial function, demonstrating significant potential in treating mature neuronal axon injuries and sciatic nerve injuries.
Keywords:
axon regeneration; energy supply; glucose metabolism; harmine; metabolic coupling; mitochondrial function; neuron.