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As senescent cells seemed to be primed for ferroptosis, we reasoned that protective mechanisms against ferroptosis must be upregulated in senescent cells

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While important mechanistic insights were gained to decipher the glutaredoxin-catalyzed reduction of glutathione disulfide substrates, there are still major gaps in our understanding of the enzyme mechanism regarding the reduction of non-glutathione disulfide substrates

However, Al-Maleki et al

This leads to the release and cytoplasmic translocation of p53, which can subsequently activate transcription-independent pro-apoptotic signaling (Figures 6A,B)

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