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Archived from the original on 13 June 2011

However, under defined pathophysiological stresses, including inflammatory cues, metal overload, cysteine deprivation, or drug exposure, GSH oxidation and thiol chemistry may become coupled to metal redox cycling and mitochondrial damage amplification, thereby increasing susceptibility to forms of regulated cell death such as ferroptosis and cuproptosis

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Some of the released molecules, referred to as damage-associated molecular patterns (DAMPs) like heme and its derivatives, ATP, heat shock protein (HSP70), or interleukin-33 (IL-33), are capable of triggering the immune response, amplifying inflammation [62, 63]

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