The cytokine transforming growth factor (TGF)-β 1 is highly induced after encephalopathic brain injury, with data showing that it can both contribute to the pathophysiology and aid in disease resolution. In the immature brain, sustained TGFβ-signaling after injury may prolong inflammation to both exacerbate acute stage damage and perturb the normal course of development. Yet in adult encephalopathy, elevated TGFβ 1 may promote a reparative state. In this review, we highlight the context-dependent actions of TGFβ-signaling in the brain during resolution of encephalopathy and focus on neuronal survival mechanisms that are affected by TGFβ 1 . We discuss the mechanisms that contribute to the disparate actions of TGFβ 1 toward elucidating the long-term neurological and neuropsychiatric consequences that follow encephalopathic injury.
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Kim et al. (2018) studied this question.
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