Delayed cell death signaling in traumatized central nervous system: Hypoxia

D. Chu, J. Qiu, M. Grafe, R. Fabian, T. A. Kent, D. Rassin, O. Nesic, K. Werrbach-Perez, R. Perez-Polo

Research output: Contribution to journalArticlepeer-review

34 Scopus citations


There are two different ways for cells to die: Necrosis and apoptosis. Cell death has traditionally been described as necrotic or apoptotic based on morphological criteria. There are controversy about the respective roles of apoptosis and necrosis in cell death resulting from trauma to the central nervous system (CNS). An evaluation of work published since 1997 in which electron microscopy was applied to ascertain the role of apoptosis and necrosis in: spinal cord injury, stroke, and hypoxia/ischemia (H/I) showed evidence for necrosis and apoptosis based on DNA degradation, presence of histones in cytoplasm, and morphological evidence in spinal cord. In the aftermath of stroke, many of the biochemical markers for apoptosis were present but the morphological determinations suggested that necrosis is the major source of post-traumatic cell death. This was not the case in H/I where both biochemical assays and the morphological studies gave more consistent results in a manner similar to the spinal cord injury studies. After H/I, major factors affecting cell death outcomes are DNA damage and repair processes, expression of bcl-like gene products and inflammation-triggered cytokine production.

Original languageEnglish (US)
Pages (from-to)97-106
Number of pages10
JournalNeurochemical Research
Issue number1-2
StatePublished - 2002
Externally publishedYes


  • Apoptosis
  • Cells death
  • Hypoxia
  • Necrosis

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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