Galectin-3 activates microglia and promotes neurological impairment via NLRP3/pyroptosis pathway following traumatic brain injury.

Background: Externally caused traumatic brain injury (TBI) poses a woeful worldwide health concern, bringing about disability, death, and prolonged neurological impairment. Increased galectin-3 levels have been linked to unfavorable outcomes in several neurological conditions. This study explores the role of galectin-3 in TBI, specifically examining its contribution to neuroinflammation.

NINJ1-mediated plasma membrane rupture of pyroptotic endothelial cells exacerbates blood-brain barrier destruction caused by neutrophil extracellular traps in traumatic brain injury.

Brain endothelial cell (bEC) dysfunction is the main factor of blood-brain barrier (BBB) breakdown, which triggers a vicious cycle of aggravating traumatic brain injury (TBI) pathogenesis. Previous studies have revealed that neutrophil extracellular traps (NETs) released by neutrophils can lead to BBB disruption, but there is a lack of research on the underlying mechanisms after TBI. Here, excessive NETs were found in both contused brain tissue and circulation following TBI.