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Traumatic neural injury mechanisms include notable down-stream consequences on excitotoxic injury, cerebral vascular flow, diffusion along axonal pathways, and activation of microglia

In whole, the data of different studies show that the concentration of 4-HNEs in the cell is important for the activation of the cell cycle and signal cascades regulating cell differentiation, proliferation, and apoptosis, the level of 4-HNEs being strongly dependent on the activity of GSTA4-4 both in the cytoplasm and in the mitochondria

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This protein interacts with RIP-associated Ich-1/Ced-3 homologous protein with a death domain (RAIDD) and recruits procaspase-2 leading to truncation of Bid by active caspase-2 and following mitochondrial outer membrane permeabilization (MOMP) and apoptosis [36]