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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Main Authors: Ten, Vadim S., Yao, Jun, Ratner, Veniamin, Sosunov, Sergey, Fraser, Deborah A., Botto, Marina, Sivasankar, Baalasubramanian, Morgan, B. Paul, Silverstein, Samuel, Stark, Raymond, Polin, Richard, Vannucci, Susan J., Pinsky, David, Starkov, Anatoly A.
Formato: Artigo
Idioma:Inglês
Publicado em: Society for Neuroscience 2010
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Articles
Acesso em linha: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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