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Glycolysis amplifies liver fibrosis by promoting the release of fibrogenic extracellular vesicles (EVs) from HSCs, particularly in the hepatic pericentral zone, highlighting glycolysis as a therapeutic target (76)

The explanation for this discrepancy can be found in recent papers showing that some cancer cell linesincluding HCT116are not affected by L-BSO or GSH synthesis inactivation because they can compensate GSH depletion by the thioredoxin (TXN) pathway 25 , and by maintaining protein homeostasis through deubiquitinating enzymes (DUB) 32

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These autoantibodies might be strongly bound with CE-modified DNA than native polymer