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Targeting autophagy for drug-induced hepatotoxicity
Translocation of phosphorylated-JNK (p-JNK) to the mitochondria enhances mitochondrial oxidative stress in mouse and humans (Xie et al., 2014
Regarding treatment strategies, it is suggested that the marked decrease in GPx1 expression may be the major mechanism of tumor sensitization to anthracyclines [93] and that GPx1 can partially inhibit doxorubicin-induced cell death-related signaling in breast cancer by interfering with the activation of the sphingomyelin-ceramide pathway [85]
In addition to its direct anticancer mechanisms, PYC attenuates MTX-induced toxicity in vital organs by reducing oxidative damage, inflammation, and histological damage
Bock, F
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