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Complement Component C1q Mediates Mitochondria-Driven Oxidative Stress in Neonatal Hypoxic–Ischemic Brain Injury
Hypoxic–ischemic (HI) brain injury in infants is a leading cause of lifelong disability. We report a novel pathway mediating oxidative brain injury after hypoxia–ischemia in which C1q plays a central role. Neonatal mice incapable of classical or terminal complement activation because of C1q or C6 de...
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Hlavní autoři: | , , , , , , , , , , , , , |
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Médium: | Artigo |
Jazyk: | Inglês |
Vydáno: |
Society for Neuroscience
2010
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Témata: | |
On-line přístup: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2821109/ https://ncbi.nlm.nih.gov/pubmed/20147536 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1523/JNEUROSCI.5249-09.2010 |
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