PERK-STING Signaling Drives Neuroinflammation in Traumatic Brain Injury

摘要

Traumatic brain injury (TBI) resulting from excessive contact in sports, blast injuries in war, or occupational hazards is a widespread public health concern. Symptoms associated with TBI include neurocognitive deficits, psychiatric disorders, and encephalopathies. Neuroinflammation plays an integral role in the pathophysiology of TBI. Although neuroinflammation is initially beneficial, because it promotes debris clearance and regeneration, prolonged neuroinflammation elicits secondary injury, leading to progressive neurodegeneration (Simon et al., 2017). Dysregulated neuroinflammation also contributes to neurodegenerative diseases, brain cancers, and neurological infections (Dickens et al., 2017; Bright et al., 2019; Doron et al., 2019). Therefore, targeted immunomodulation is an actively pursued therapeutic avenue for treating these conditions. Such strategies aim to restrict acute inflammation to protective levels, prevent chronic neuroinflammation, and maximize regenerative programs.