Mitochondria in neurogenesis: Implications for mitochondrial diseases,STEM CELLS

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Mitochondria in neurogenesis: Implications for mitochondrial diseases
STEM CELLS ( IF 4.0 ) Pub Date : 2021-06-05 , DOI: 10.1002/stem.3425
Dario Brunetti _{1,

2} , Werner Dykstra ₃ , Stephanie Le ₄ , Annika Zink ₄ , Alessandro Prigione _{3,

4}

Affiliation

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.

中文翻译：

神经发生中的线粒体：对线粒体疾病的影响

线粒体是细胞器，在细胞稳态中具有公认的关键作用，包括生物能量学、氧化还原、钙信号传导和细胞死亡。鉴于人类大脑的高能量需求，线粒体对于神经元功能至关重要。因此，影响氧化磷酸化 (OXPHOS) 的线粒体疾病通常表现出神经损伤。新出现的证据表明，线粒体不仅对成熟的有丝分裂后神经元很重要，而且对神经发生过程中神经祖细胞 (NPC) 的调节也很重要。这些最近的发现将线粒体作为大脑发育过程中细胞命运决定的中心调节器。OXPHOS 突变可能会破坏 NPC 的功能，从而损害神经命运承诺所需的代谢程序。

更新日期：2021-06-05

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