Traumatic brain injuries represent the leading cause of death and morbidity in young adults in western
countries, and are responsible for a major social and economical burden. For decades, the mainstay of neurotrauma
management has been represented by control of post-traumatic edema. With the emergence of a better understanding of
the underlying cellular mechanisms responsible for the generation of secondary brain damage, the hope for the "magic
bullet" has prompted the development of novel drugs that have repeatedly failed to significantly improve outcome of
head-injured patients. During the past decade, mitochondrial functional and structural impairment has emerged as a
pivotal event in the pathway of cell to secondary death. Extensive research has identified a vast range of deleterious
signals that are generated and integrated at the mitochondrial level resulting in impairment of major mitochondrial
functions such as calcium homeostasis, free radicals generation and detoxification, energy production and
neurosteroidogenesis. Mitochondria have therefore emerged as a potential therapeutic target. Within the spectrum of
major mitochondrial structural components, the 18 kDa translocator protein (TSPO) has shown important and relevant
functions such as steroid synthesis and modulation of the mitochondrial permeability transition that may substantially
affect the fate of injured cells. This review summarizes the potential therapeutic implications of TSPO modulation in
traumatic brain injury in the view of the current knowledge on this intriguing mitochondrial complex.
Keywords: Mitochondria, 18 kDa translocator protein, mitochondrial permeability transition pore, traumatic brain injury.
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