Inflammatory and apoptotic signaling after spinal cord injury

Research output: Contribution to journalReview article

75 Scopus citations

Abstract

Central nervous system (CNS) destruction in spinal cord injury (SCI) is caused by a complex series of cellular and molecular events. Recent studies have concentrated on signaling by receptors in the tumor necrosis factor receptor (TNFR) superfamily that mediate diverse biological outcomes ranging from inflammation to apoptosis. From the perspective of basic science research, understanding how receptor signaling mediates these divergent responses is critical in clarifying events underlying irreversible cell injury in clinically relevant models of SCI. From a clinical perspective, this work also provides novel targets for the development of therapeutic agents that have the potential to protect the spinal cord from irreversible damage and promote functional recovery. In this review, we discuss how the formation of alternate signaling complexes and receptor membrane localization after SCI can influence life and death decisions of cells stimulated through two members of the TNFR superfamily, Fas/CD95 and TNFR1.

Original languageEnglish (US)
Pages (from-to)335-344
Number of pages10
JournalJournal of neurotrauma
Volume23
Issue number3-4
DOIs
StatePublished - Mar 1 2006

Keywords

  • Alternate signaling complexes
  • Neuron cell death pathways
  • Spinal cord injury
  • Tumor necrosis factor receptor

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

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