Advances in Astrocyte Research on Neuronal Death and Regeneration
The onset and progression of central nervous system (CNS) disorders are frequently associated with aberrant neuronal death. In addition to the classical forms of cell death such as apoptosis and necrosis, neurons can also undergo alternative modes of death, including ferroptosis, cuproptosis, and ammonia-induced cell death, all of which may involve the participation of astrocytes. Neuronal death is an irreversible process and plays a central role in the pathogenesis of numerous CNS diseases. We found that astrocytes exhibit the capacity to regenerate into neurons, a characteristic that may pave the way for novel therapeutic approaches in the treatment of neurological disorders. Astrocytes represent optimal starting cells for reprogramming techniques due to their anatomical proximity to neurons and their shared origin from common progenitor cells-radial glial cells. Reprogramming techniques encompass the conversion of astrocytes into pluripotent neurospheres or their direct <i>in vivo</i> reprogramming into functional neurons, aiming to replace damaged or lost neurons through processes such as transdifferentiation and dedifferentiation. This article examines the interplay between astrocytes and neuronal survival and degeneration in CNS disorders, as well as two reprogramming strategies for converting astrocytes into neurons, with the aim of establishing a scientific foundation for neuronal repair in the treatment of CNS diseases.
Authors
- Cheng null Yuan
- Ying-jiao null Liu
- Ming-rui null Liu
- Li-yuan null Cui
- Hao null Wu
- Wen-xuan null Cao
Institutions
- Jiangxi University of Traditional Chinese Medicine (CN)
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Ocean University of China (CN)
Publication Details
- Journal
- Journal of Integrative Neuroscience
- Published
- 2025-12-18
- DOI
- https://doi.org/10.31083/jin42985
- Primary Topic
- Pluripotent Stem Cells Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00