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This special interplay further highlights that the loss of any one system can overwhelm the compensatory capacity of the others, forcing the CNS into a state of redox imbalance, glial activation, and progressive inflammation (Figure 1)

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This mechanism plays a role in activating various downstream pathways, including RAS/MAPK, PI3K/AKT, Wnt/β-catenin, and JAK/STAT, which are crucial for controlling a range of cellular physiological activities such as differentiation, proliferation, epithelial cell movement, angiogenesis, and EMT [21]

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