Mitochondria in neurogenesis: Implications for mitochondrial diseases

During healthy neurogenesis, there is an orchestrated programming of energy metabolism, which transits from glycolysis toward oxidative phosphorylation (OXPHOS). In mitochondrial diseases, neural progenitor cells (NPCs) may fail to acquire an OXPHOS profile, leading to impaired generation and maturation of neurons. NPC metabolism may thus represent a potential target of interventions for mitochondrial neurological diseases. AbstractMitochondria are organelles with recognized key roles in cellular homeostasis, including bioenergetics, redox, calcium signaling, and cell death. Mitochondria are essential for neuronal function, given the high energy demands of the human brain. Consequently, mitochondrial diseases affecting oxidative phosphorylation (OXPHOS) commonly exhibit neurological impairment. Emerging evidence suggests that mitochondria are important not only for mature postmitotic neurons but also for the regulation of neural progenitor cells (NPCs) during the process of neurogenesis. These recent findings put mitochondria as central regulator of cell fate decisions during brain development. OXPHOS mutations may disrupt the function of NPCs and thereby impair the metabolic programming required for neural fate commitment. Promoting the mitochondrial function of NPCs could therefore represent a novel interventional approach against incurable mitochondrial diseases.
Source: Stem Cells - Category: Stem Cells Authors: Tags: Tissue ‐Specific Stem Cells Source Type: research