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• W61765403 abstract "Hypoxic-ischemic brain injury remains a leading cause of mortality and morbidity in neonates. The inflammatory response, which is characterized in part by activation of local immune cells, has been implicated as a core component for the progression of damage to the immature brain following hypoxia-ischemia (HI). However, mounting evidence implicates circulating immune cells recruited to the site of damage as orchestrators of neuron-glial interactions and perpetuators of secondary brain injury. This suggests that re-directing our attention from the local inflammatory response toward the molecular mediators believed to link brain-immune cell interactions may be a more effective approach to mitigating the inflammatory sequelae of perinatal HI. In this review, we focus our attention on cyclooxygenase-2, a mediator by which peripheral immune cells may modulate signaling pathways in the brain that lead to a worsened outcome. Additionally, we present an overview of emerging therapeutic modalities that target mechanisms of neuroinflammation in the hypoxic-ischemic neonate." @default.
• W61765403 created "2016-06-24" @default.
• W61765403 creator A5016467704 @default.
• W61765403 creator A5018864580 @default.
• W61765403 creator A5023710328 @default.
• W61765403 creator A5071071190 @default.
• W61765403 date "2011-01-01" @default.
• W61765403 modified "2023-10-07" @default.
• W61765403 title "The Evolving Landscape of Neuroinflammation After Neonatal Hypoxia-Ischemia" @default.
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• W61765403 doi "https://doi.org/10.1007/978-3-7091-0693-8_15" @default.
• W61765403 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21725737" @default.
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