The bioenergetics of traumatic brain injury and its long-term impact for brain plasticity and function

Pharmacol Res. 2024 Oct:208:107389. doi: 10.1016/j.phrs.2024.107389. Epub 2024 Sep 5.

Abstract

Mitochondria provide the energy to keep cells alive and functioning and they have the capacity to influence highly complex molecular events. Mitochondria are essential to maintain cellular energy homeostasis that determines the course of neurological disorders, including traumatic brain injury (TBI). Various aspects of mitochondria metabolism such as autophagy can have long-term consequences for brain function and plasticity. In turn, mitochondria bioenergetics can impinge on molecular events associated with epigenetic modifications of DNA, which can extend cellular memory for a long time. Mitochondrial dysfunction leads to pathological manifestations such as oxidative stress, inflammation, and calcium imbalance that threaten brain plasticity and function. Hence, targeting mitochondrial function may have great potential to lessen the outcomes of TBI.

Keywords: 7,8-DHF (PubChem CID: 38183–03-8); Bumetanide (PubChem CID: 2471); Cyclosporin (PubChem CID: 5284373); Dexmedetomidine (PubChem CID: 5311068); Epigenetic; Etifoxine (PubChem CID: 135413553); Hunanin (PubChem CID: 16135997); Inflammation; Kaempferol (PubChem CID: 5280863); MCC950 (PubChem CID: 9910393); Melatonin (PubChem CID: 896); Minocycline (PubChem CID: 54675783); Mitochondrial dynamics; Mitophagy; Pramipexole (PubChem CID: 119570); Quercetin (PubChem CID: 5280343); R13 (PubChem CID: 90117609); Rapamycin (PubChem CID: 5284616); Resolvin D1 (PubChem CID: 44251266); Ru360 (PubChem CID: 85392867); SS-31 (PubChem CID: 11764719); Salubrinal (PubChem CID: 5717801); Sevoflurane (PubChem CID: 5206); Traumatic brain injury; Triiodothyronine (PubChem CID: 5920); oxidative stress.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain Injuries, Traumatic* / metabolism
  • Brain Injuries, Traumatic* / physiopathology
  • Brain* / metabolism
  • Brain* / pathology
  • Brain* / physiopathology
  • Energy Metabolism*
  • Humans
  • Mitochondria* / metabolism
  • Neuronal Plasticity*
  • Oxidative Stress