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Although none of the studies reviewed the cross between cuproptosis and apoptosis, autophagy, necroptosis and pyroptosis, some clues offer the possibility

By inducing excessive oxidative stress, NPC1L1 inhibition increased treatment cytotoxicity and sharply decreased the number of persisters, whereas recovering the key substrates of NPC1L1, cholesterol, and vitamin E, markedly compromised lipotoxicity-mediated oxidative stress

Altogether, our findings suggest that IGF1R depletion in the lung TME of IGF1R-deficient mice delays lung metastasis implantation and progression by reducing the presence of blood vessels, fibroblasts, TAMs and FOXP3 + TILs, as well as by increasing the amount of infiltrating CD4 + and CD8 + T cells (Fig

Vaario LM, Fritze H, Spetz P, Heinonsalo J, Hanajik P, Pennanen T