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The resulting damage intensifies cellular dysfunction and suppresses mitochondrial respiration, thereby aggravating the bioenergetic failure that underlies severe sepsis (Vctor et al., 2009
Genetic variations in the activity of glutathione-S-transferase-4, a GSH-dependent enzyme that reduces 4hydroxynonenal, is a determining factor in the extent of neurodegeneration after TBI (Al Nimer et al., 2013)
IGF-1 LR3 binds to IGF-1 receptors on muscle cells, activating pathways like PI3K/Akt/mTOR that promote muscle growth and inhibit muscle breakdown
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