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In pathological conditions, astrocytes undergo significant molecular and morphological remodeling, adopting either a detrimental A1 (neurotoxic) or beneficial A2 (neuroprotective) reactive state that, respectively, drives injury progression or promotes tissue repair [132, 133]

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It is possible that mutation of the iron-binding histidines changes the tertiary structure of CDO in such a way that it is no longer recognized by an ubiquitin ligase, resulting in the disruption of cysteine-sensitive ubiquitination and degradation