Open AccessMitochondria in neurogenesis: Implications for mitochondrial diseases
Author(s) -
Brunetti Dario,
Dykstra Werner,
Le Stephanie,
Zink Annika,
Prigione Alessandro
Publication year - 2021
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1002/stem.3425
Subject(s) - neurogenesis , mitochondrion , biology , microbiology and biotechnology , oxidative phosphorylation , bioenergetics , neural stem cell , cell fate determination , regulator , progenitor cell , stem cell , neuroscience , biochemistry , transcription factor , gene
Mitochondria 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.