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Pediatr Infect Dis J.2018;37(8):749-754

Other enzymes, such as AARS and alpha-tubulin ACT1 (ATAT1) have also been found to play a role

early life stress or chronic drug exposure [15,16,17], may lead to redox dysfunction and chronic oxidative stress, strongly linked to the pathophysiology of schizophrenia [18,19,20,21,22]

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Beyond the canonical GPX4-glutathione (GSH) axis, recent studies have identified additional protective mechanisms such as ferroptosis suppressor protein 1 (FSP1), guanosine triphosphate cyclohydrolase 1 (GCH1), and mitochondrial dihydroorotate dehydrogenase (DHODH), which provide complementary safeguards against ferroptotic death