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Death Receptors in Acute Brain Injury

  • Chapter
Brain Injury

Part of the book series: Molecular and Cellular Biology of Critical Care Medicine ((MCCM,volume 2))

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Abstract

It is now known that cell death following acute and chronic insults to the central nervous system (CNS) is mediated by death programs involving activation of caspases (Beattie et al. 2000; Eldadah et al. 2000; Fiskum 2000; MacManus et al. 2000; Raghupathi et al. 2000; Yuan et al. 2000; Zipfel et al. 2000). Although the cellular events downstream of activated caspases have been the subject of intense study, the exact mechanisms that initiate activation of cell death programs after acute CNS injury are less clear. Death receptors are transmembrane, multi-domain proteins that, when activated by specific ligands, initiate caspase cascades and apoptotic cell death in T-lymphocytes and natural killer cells following an immune response (Nagata 1997). Recent studies have suggested that death receptor signaling may initiate caspase cascades and cell death in the CNS during development and following ischemia, trauma, and neurodegenerative diseases (Martin-Villalba et al. 1999; Beer et al. 2000; Raoul et al. 2000). If so, then death receptors or their signaling pathways may represent novel targets for therapies aimed at limiting damage after acute or chronic CNS injury. This chapter will provide a general review of death receptors and their signaling mechanisms, focusing on the two best characterized death receptors, Fas and TNF-α.

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Whalen, M.J., Moskowitz, M.A. (2001). Death Receptors in Acute Brain Injury. In: Clark, R.S.B., Kochanek, P. (eds) Brain Injury. Molecular and Cellular Biology of Critical Care Medicine, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1721-4_9

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  • DOI: https://doi.org/10.1007/978-1-4615-1721-4_9

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