By combining mechanistic studies with translational perspectives, this review highlights that astrocytes act as central mediators of secondary injury and repair in TBI pathology. Given the context-dependent nature of astrocyte signaling, future therapeutic strategies should aim to reprogram astrocyte responses with temporal and cell-type precision rather than pursuing broad inhibition. Also, targeting astrocyte-specific pathways, such as the TLR4 and NF-κB pathways, may mitigate secondary injury and improve outcomes. This underscores the therapeutic potential of modulating astrocyte responses in the treatment of TBI.
Wu et al. (Wed,) studied this question.
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