TGFβ1: Friend or Foe During Recovery in Encephalopathy

Abstract

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.

Keywords: TGFβ; birth asphyxia; cell death; encephalopathy; neuroinflammation; neuroprotection.