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Mitochondria in traumatic brain injury and mitochondrial‐targeted multipotential therapeutic strategies
Author(s) -
Cheng Gang,
Kong Ronghua,
Zhang Leiming,
Zhang Jianning
Publication year - 2012
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.2012.02025.x
Subject(s) - excitotoxicity , mitochondrion , traumatic brain injury , programmed cell death , apoptosis , neuroscience , caspase , brain damage , cell damage , cell , microbiology and biotechnology , neuroprotection , medicine , apoptosis inducing factor , oxidative stress , biology , bioinformatics , psychiatry , biochemistry
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.