Table 1.
The role of nutrient-sensing and metabolic pathways/protein homeostasis in NSCs from quiescence to activity
| Role | qNSCs | aNSCs |
|---|---|---|
| Nutrient-sensing and metabolic pathways | ||
| Nutrient-sensing pathways | Activation of FOXO | Move FOXO out of the nucleus |
| Oxygen sensing | Stable HIF-1α | Enhanced HIF-1α |
| Glucose metabolism | Glycolysis and glutamine catabolism | Oxidative phosphorylation |
| Mitochondrial dynamics | Elongated fused morphology | Smaller and more fragmented morphology |
| Lipid metabolism | Prefer FA oxidation | Prefer lipid synthesis |
| Protein homeostasis | ||
| Autophagy-lysosomal pathway | Higher lysosomal activity | Stable lysosomal activity |
| Proteasome pathway | More sensitive | Less sensitive |
| Chaperones | Energy-consuming TriC | Non-energy-consuming HspB5 |
aNSCs: Active NSCs; FOXO: forkhead box protein O; HIF: hypoxia-inducible factor; NSCs: neural stem cells; qNSCs: quiescent NSCs.