p66shc's role as an essential mitophaghic molecule in controlling neuronal redox and energetic tone

Amy M. Kleman, Jacquelynn E. Brown, Stephanie L.H. Zeiger, Jane C. Hettinger, Joshua D. Brooks, Benjamin Holt, Jason D. Morrow, Erik S. Musiek, Ginger L. Milne, Beth Ann McLaughlin

Research output: Contribution to journalShort survey

5 Scopus citations

Abstract

Stroke is the leading cause of adult disability in the U.S. and is now recognized as a global epidemic. There are currently no FDA-approved drugs to block the cell death that results from oxygen and glucose deprivation. This void in clinical medicine has sparked an intense interest in understanding endogenous cellular protective pathways that might be exploited for therapeutic development. The work highlighted here describes the critical role between redox tone and energetic stress signaling in mediating mitophagy and determining neuronal cell fate following acute oxygen glucose deprivation.

Original languageEnglish
Pages (from-to)948-949
Number of pages2
JournalAutophagy
Volume6
Issue number7
DOIs
StatePublished - Oct 1 2010
Externally publishedYes

Keywords

  • Hypoxia
  • Ischemia
  • Mitochondria
  • Mitophagy
  • Neurodegeneration
  • Preconditioning

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    Kleman, A. M., Brown, J. E., Zeiger, S. L. H., Hettinger, J. C., Brooks, J. D., Holt, B., Morrow, J. D., Musiek, E. S., Milne, G. L., & McLaughlin, B. A. (2010). p66shc's role as an essential mitophaghic molecule in controlling neuronal redox and energetic tone. Autophagy, 6(7), 948-949. https://doi.org/10.4161/auto.6.7.13007