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Central mechanisms driving this secondary damage include vascular disruption and ischemia, excitotoxicity mediated by excessive glutamate, oxidative stress, lipid peroxidation, and the release of proinflammatory cytokines and signaling molecules, which create a pro-inflammatory microenvironment (Eftekharpour et al., 2008

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Therefore, the focus of the field is turning towards understanding the interplay between transplants and the subacute/secondary brain injury environment

During ischemia, oxygen deprivation leads to ATP depletion and impaired Na/K-ATPase activity within tubular epithelial cells, particularly in the medullary thick ascending limb

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Impaired Amino Acid Transport at the Blood Brain Barrier Is a Cause of Autism Spectrum Disorder