Mitochondrial damage in traumatic CNS injury

W. Brad Hubbard, Laurie M. Davis, Patrick G. Sullivan

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

7 Scopus citations


Traumatic brain injury (TBI) is ever-present in societal issues and puts a tremendous economic burden on U.S. healthcare and affected individuals. Symptomology after TBI is sometimes subtle without outward signs of injury and neurological impairments can be long-lasting. Unfortunately, the underlying cellular mechanisms that occur in response to TBI have not fully been deduced and as such there is no FDA-approved treatment for the resulting neurological pathology. In this chapter, we will review the essential role of mitochondria in the CNS while highlighting numerous functions of this crucial organelle under basal conditions. Furthermore, we review the bevy of literature showing the dysfunction of mitochondria after TBI. After TBI, these normal mitochondrial functions become dysregulated in response to elevated Ca2+ mitochondrial buffering and further cause downstream damage. The loss of adequate membrane potential can lead to lower ATP levels and necrotic cell death. Ca2+ overload also leads to the formation of the mitochondrial permeability transition pore and cytochrome c-mediated apoptosis. Aberrant levels of reactive oxygen species resultant from mitochondrial dysfunction cause increased lipid peroxidation and presence of 4-hydroxynonenal. All of these secondary cascades involved in mitochondrial dysfunction present unique therapeutic targets that investigators throughout the years have evaluated. The development of new pharmacological tools, with translatable potential, targeting mitochondrial pathways will further validate the critical role of mitochondria in outcomes after TBI and hopefully advance research to find an effective treatment.

Original languageEnglish
Title of host publicationAcute Neuronal Injury
Subtitle of host publicationThe Role of Excitotoxic Programmed Cell Death Mechanisms: Second Edition
Number of pages19
ISBN (Electronic)9783319774954
StatePublished - Jan 1 2018

Bibliographical note

Publisher Copyright:
© Springer International Publishing AG, part of Springer Nature 2010, 2018.


  • Cell death
  • Electron transport chain
  • Mitochondria
  • Reactive oxygen species
  • Traumatic brain injury

ASJC Scopus subject areas

  • Medicine (all)
  • Neuroscience (all)
  • Biochemistry, Genetics and Molecular Biology (all)
  • Agricultural and Biological Sciences (all)


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