The cytokine transforming growth factor (TGF)-β₁ 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 TGFβ₁ 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 TGFβ₁. We discuss the mechanisms that contribute to the disparate actions of TGFβ₁ toward elucidating the long-term neurological and neuropsychiatric consequences that follow encephalopathic injury.

细胞因子转化生长因子（TGF）-β ₁脑病脑损伤后高度诱导，有数据显示，它既能有助于解决疾病的病理生理和援助。在未成熟的大脑中，损伤后持续的TGFβ信号传导可能会延长炎症，从而加剧急性期损伤并扰乱正常的发育过程。然而，在成人性脑病，提高TGFβ ₁可促进修复状态。在这次审查中，我们由TGFβ影响了神经元的存活机制性脑病和重点解决过程中突出显示大脑TGFβ信号传导的依赖于上下文的动作₁。我们讨论有助于TGFβ的不同行为的机制₁ 阐明脑病性损伤后的长期神经病学和神经精神病学后果。