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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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Archived from the original on 13 June 2011

Mouse models are highly effective in age related studies as the shortened timeline allows observation of the full impact of treatments in months as opposed to the years of human clinical trials

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