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47,48 These glial pathologies can be theoretically important for a discussion of GABA neurotransmission from the perspective that glial cells, such as astrocytes, regulate glutamate–glutamine cycling through cellular machinery that includes EAAT1/2 and glutamine synthetase (see earlier discussion on Glutamate inactivation and catabolism)
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Previously, we showed that TG2 mediates crystallin, caspase 3, and collagen crosslinking in response to oxidative stress, hypoxic stress, and DNA damage, which leads to cataract formation, apoptotic resistance, and fibrotic development, respectively 4,5,6
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