NG2 cells are highly proliferative glial cells that can self-renew or differentiate into oligodendrocytes, promoting remyelination. Following demyelination, the proliferative and differentiation potentials of NG2 cells increase rapidly, enhancing their differentiation into functional myelinating cells. Levels of the transcription factors Olig1 and Olig2 increase during the differentiation of NG2 cells and play important roles in the development and repair of oligodendrocytes. However, the ability to generate new oligodendrocytes is hampered by injury-related factors (e.g., myelin fragments, Wnt and Notch signaling components), leading to failed differentiation and maturation of NG2 cells into oligodendrocytes. Here, we review Notch signaling as a negative regulator of oligodendrocyte differentiation and discuss the extracellular ligands, intracellular pathways, and key transcription factors involved.

NG2细胞是高度增殖的神经胶质细胞，可以自我更新或分化为少突胶质细胞，促进髓鞘再生。脱髓鞘后，NG2 细胞的增殖和分化潜能迅速增加，增强了它们向功能性髓鞘细胞的分化。转录因子 Olig1 和 Olig2 的水平在 NG2 细胞分化过程中增加，并在少突胶质细胞的发育和修复中起重要作用。然而，产生新的少突胶质细胞的能力受到损伤相关因素的阻碍（例如.、髓鞘片段、Wnt 和 Notch 信号成分），导致 NG2 细胞无法分化和成熟为少突胶质细胞。在这里，我们回顾了 Notch 信号作为少突胶质细胞分化的负调节因子，并讨论了细胞外配体、细胞内通路和所涉及的关键转录因子。