Abstract
Background Neonatal hypoxia-ischemia (HI) is a common cause of morbidity and mortality in neonates. It can result in persistent motor, sensory, and cognitive impairments. Recent evidence suggests that the transcription factor hypoxia-inducible factor 1α (HIF-1α) plays a key role in neurological outcomes after HI. Microglia are brain resident macrophages that respond rapidly to HI by producing proinflammatory mediators via a HIF-1α-dependent mechanism. However, the precise role of HIF-1α – dependent repair and damage mechanisms on the formation of brain injury after a hypoxic-ischemic brain event in microglia is still poorly understood.
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