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Comment
. 2022 May;32(5):417-418.
doi: 10.1038/s41422-022-00653-7.

Cuproptosis: a copper-triggered modality of mitochondrial cell death (V体育官网入口)

Daolin Tang  1 , Xin Chen  2 , Guido Kroemer  3   4   5
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Cuproptosis: a copper-triggered modality of mitochondrial cell death

Daolin Tang et al. Cell Res. 2022 May.
No abstract available

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Figures

Fig. 1
Fig. 1. Signaling and mechanism of cuproptosis.
Elesclomol binds copper (Cu2+) in the extracellular environment and transports it to intracellular compartments. Increased Cu accumulation causes cuproptosis mainly through FDX1-mediated mitochondrial proteotoxic stress. On the one hand, FDX1 reduces Cu2+ to Cu+, facilitating the lipoylation (LA) and aggregation of enzymes (especially DLAT) involved in the regulation of mitochondrial TCA cycle. On the other hand, FDX1 causes the destabilization of Fe–S cluster proteins. In addition to Cu ionophores, Cu importers (e.g., SLC31A1) and exporters (e.g., ATP7B) regulate cuproptosis sensitivity by affecting intracellular Cu+ levels. GSH functions as a thiol-containing copper chelator that blocks cuproptosis, whereas BSO promotes cuproptosis by depleting GSH. The mitochondrial pyruvate carrier (MPC) inhibitor UK5099 and electron transport chain (ETC) complex I/III inhibitors (e.g., rotenone and antimycin A) attenuate elesclomol-induced cuproptosis.
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References

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