Mitochondria and microRNA crosstalk in traumatic brain injury

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17 Scopus citations


Traumatic brain injury (TBI) is a leading cause of long-term impairments in higher cognitive functioning, including deficits in attention and memory. It is well known that some of these persistent deficits are related, in part, to ongoing secondary injury events characterized by pervasive biochemical and pathophysiological stressors, including a rapid and sustained phase of mitochondrial dysfunction. A loss of mitochondrial function impacts a number of important cellular events and we have begun to investigate the novel hypothesis that mitochondria play a critical role in regulating the cellular activity of specific microRNAs in response to cellular demands and stressors. In this special issue report, we summarize briefly the rationale for investigating the crosstalk between mitochondria and microRNA, and provide recent preliminary data suggesting that mitochondria–microRNA interactions are modified in response to TBI-related cellular stressors. We postulate that this interaction is critical for regulating appropriate cellular microRNA responses, which opens up opportunities for therapeutic interventions targeting both mitochondrial function and microRNA activity.

Original languageEnglish
Pages (from-to)104-108
Number of pages5
JournalProgress in Neuro-Psychopharmacology and Biological Psychiatry
StatePublished - Feb 6 2017


  • Glutamate excitotoxicity
  • Mitochondrial function
  • Oxidative damage
  • Traumatic brain injury

ASJC Scopus subject areas

  • Pharmacology
  • Biological Psychiatry


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