Regulation of adult neurogenesis: the crucial role of astrocytic mitochondria.

IF 3.5 3区 医学 Q2 NEUROSCIENCES
Frontiers in Molecular Neuroscience Pub Date : 2024-11-22 eCollection Date: 2024-01-01 DOI:10.3389/fnmol.2024.1516119
Danping Liu, Pei Guo, Yi Wang, Weihong Li
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引用次数: 0

Abstract

Neurogenesis has emerged as a promising therapeutic approach for central nervous system disorders. The role of neuronal mitochondria in neurogenesis is well-studied, however, recent evidence underscores the critical role of astrocytic mitochondrial function in regulating neurogenesis and the underlying mechanisms remain incompletely understood. This review highlights the regulatory effects of astrocyte mitochondria on neurogenesis, focusing on metabolic support, calcium homeostasis, and the secretion of neurotrophic factors. The effect of astrocytic mitochondrial dysfunction in the pathophysiology and treatment strategies of Alzheimer's disease and depression is discussed. Greater attention is needed to investigate the mitochondrial autophagy, dynamics, biogenesis, and energy metabolism in neurogenesis. Targeting astrocyte mitochondria presents a potential therapeutic strategy for enhancing neural regeneration.

成人神经发生的调控:星形细胞线粒体的关键作用。
神经发生已成为治疗中枢神经系统疾病的一种很有前途的方法。神经元线粒体在神经发生中的作用已被充分研究,然而,最近的证据强调星形细胞线粒体功能在调节神经发生中的关键作用,其潜在机制仍不完全清楚。本文综述了星形胶质细胞线粒体在神经发生中的调节作用,重点介绍了代谢支持、钙稳态和神经营养因子的分泌。本文讨论了星形细胞线粒体功能障碍在阿尔茨海默病和抑郁症的病理生理和治疗策略中的作用。神经发生过程中线粒体自噬、动力学、生物发生和能量代谢等方面的研究有待进一步深入。靶向星形胶质细胞线粒体是一种潜在的增强神经再生的治疗策略。
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来源期刊
CiteScore
5.70
自引率
2.10%
发文量
669
审稿时长
14 weeks
期刊介绍: Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.
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