Mitochondria in traumatic brain injury and mitochondrial-targeted multipotential therapeutic strategies

Br J Pharmacol. 2012 Oct;167(4):699-719. doi: 10.1111/j.1476-5381.2012.02025.x.

Abstract

Traumatic brain injury (TBI) is a major health and socioeconomic problem throughout the world. It is a complicated pathological process that consists of primary insults and a secondary insult characterized by a set of biochemical cascades. The imbalance between a higher energy demand for repair of cell damage and decreased energy production led by mitochondrial dysfunction aggravates cell damage. At the cellular level, the main cause of the secondary deleterious cascades is cell damage that is centred in the mitochondria. Excitotoxicity, Ca(2+) overload, reactive oxygen species (ROS), Bcl-2 family, caspases and apoptosis inducing factor (AIF) are the main participants in mitochondria-centred cell damage following TBI. Some preclinical and clinical results of mitochondria-targeted therapy show promise. Mitochondria- targeted multipotential therapeutic strategies offer new hope for the successful treatment of TBI and other acute brain injuries.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain Injuries / drug therapy
  • Brain Injuries / metabolism*
  • Brain Injuries / pathology
  • Cell Death
  • Humans
  • Mitochondria / metabolism*
  • Neurons / metabolism
  • Neurons / pathology
  • Reactive Oxygen Species / metabolism

Substances

  • Reactive Oxygen Species