Traumatic brain injury (TBI) is still the worldwide, leading cause of mortality and morbidity in young adults.
The prognosis of TBI patients is strongly affected by secondary brain damage including mitochondrial dysfunctions. In
many basic and clinical studies, mitochondrial dysfunctions, including the opening of mitochondrial permeability
transition (mPT) pore, and treatments including cyclosporine A (CsA) have been studied. These evidences suggest an
important role for mitochondria as therapeutic targets for neuroprotection after TBI.
This review summarizes the data about normal and pathological mitochondrial function after TBI, TBI pathobiology
relating to mitochondrial dysfunction and therapeutic strategies including drug treatment. This review also mentioned
about glucose, lactate, and pyruvate metabolisms in TBI, including the "astrocyte-neuron lactate shuttle (ANLS)"
hypothesis. Mitochondrial pathophysiology in TBI is still unclear.
Thus, the pharmacological treatment in TBI patient is still challenging. This review could help further understanding of
this topic. Hopefully, this could help further development and innovation for drug therapies in TBI.