Mitochondrial dysfunction contributes to cell death following traumatic brain injury in adult and immature animals

Research output: Contribution to journalArticle

Abstract

Secondary injury following traumatic brain injury (TBI) is characterized by a variety of pathophysiologic cascades. Many of these cascades can have significant detrimental effects on cerebral mitochondria. These include exposure of neurons to excitotoxic levels of excitatory neurotransmitters with intracellular calcium influx, generation of reactive oxygen species, and production of peptides that participate in apoptotic cell death. Both experimental and clinical TBI studies have documented mitochondrial dysfunction, and animal studies suggest this dysfunction begins early and may persist for days following injury. Furthermore, interventions targeting mitochondrial mechanisms have shown neuroprotection after TBI. Continued evaluation and understanding of mitochondrial mechanisms contributing to neuronal cell death and survival after TBI is indicated. In addition, important underlying factors, such as brain maturation, that influence mitochondrial function should be studied. The ability to identify, target, and manipulate mitochondrial dysfunction may lead to the development of novel therapies for the treatment of adult and pediatric TBI.

Original languageEnglish (US)
Pages (from-to)363-368
Number of pages6
JournalJournal of Bioenergetics and Biomembranes
Volume36
Issue number4 SPEC.ISS.
DOIs
StatePublished - Aug 2004
Externally publishedYes

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Cell Death
Wounds and Injuries
Neurotransmitter Agents
Reactive Oxygen Species
Cell Survival
Mitochondria
Traumatic Brain Injury
Pediatrics
Calcium
Neurons
Peptides
Brain
Therapeutics

Keywords

  • apoptosis
  • bcl-2
  • Brain mitochondria
  • cytochrome c
  • development
  • membrane permeability transition
  • pediatric

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

Cite this

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abstract = "Secondary injury following traumatic brain injury (TBI) is characterized by a variety of pathophysiologic cascades. Many of these cascades can have significant detrimental effects on cerebral mitochondria. These include exposure of neurons to excitotoxic levels of excitatory neurotransmitters with intracellular calcium influx, generation of reactive oxygen species, and production of peptides that participate in apoptotic cell death. Both experimental and clinical TBI studies have documented mitochondrial dysfunction, and animal studies suggest this dysfunction begins early and may persist for days following injury. Furthermore, interventions targeting mitochondrial mechanisms have shown neuroprotection after TBI. Continued evaluation and understanding of mitochondrial mechanisms contributing to neuronal cell death and survival after TBI is indicated. In addition, important underlying factors, such as brain maturation, that influence mitochondrial function should be studied. The ability to identify, target, and manipulate mitochondrial dysfunction may lead to the development of novel therapies for the treatment of adult and pediatric TBI.",
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