PTEN/PI3K and MAPK signaling in protection and pathology following CNS injuries

Research output: Contribution to journalReview article

23 Scopus citations


Brain and spinal cord injuries initiate widespread temporal and spatial neurodegeneration, through both necrotic and programmed cell death mechanisms. Inflammation, reactive oxidation, excitotoxicity and cell-specific dysregulation of metabolic processes are instigated by traumatic insult and are main contributors to this cumulative damage. Successful treatments rely on prevention or reduction of the magnitude of disruption, and interfering with injurious cellular responses through modulation of signaling cascades is an effective approach. Two intracellular signaling pathways, the phosphatase and tensin homolog (PTEN)/phosphatidylinositol 3-kinase (PI3K) and mitogenactivated protein kinase (MAPK) signaling cascades play various cellular roles under normal and pathological conditions. Activation of both pathways can influence anatomical and functional outcomes in multiple CNS disorders. However, some mechanisms involve inhibiting or enhancing one pathway or the other, or both, in propagating specific downstream effects. Though many intracellular mechanisms contribute to cell responses to insult, this review examines the evidence exploring PTEN/PI3K and MAPK signaling influence on pathology, neuroprotection, and repair and how these pathways may be targeted for advancing knowledge and improving neurological outcome after injury to the brain and spinal cord.

Original languageEnglish (US)
Pages (from-to)421-433
Number of pages13
JournalFrontiers in Biology
Issue number4
StatePublished - Aug 1 2013


  • axon regeneration
  • MAPK
  • neuroprotection
  • PTEN
  • spinal cord injury
  • traumatic brain injury

ASJC Scopus subject areas

  • Ecology, Evolution, Behavior and Systematics
  • Biotechnology
  • Genetics
  • Ecology

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