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this strategy provides a clear blueprint for combining GSH-sensing motifs with organelle-specific drug release to increase tumor selectivity and potency [20]
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Its expression is significantly elevated in breast cancer and various other drug-resistant tumors ( - can be activated by several stress conditions, including amino acid deprivation, electrophiles, oxidative stress, glucose starvation, and factors dependent on NRF2 and ATF4 ( - expression by inhibiting SLC7A11, thereby influencing ferroptosis ( - contributing to sorafenibs efficacy in drug-resistant cancers ( - , facilitates the exchange of intracellular glutamate for extracellular cysteine, a process essential for maintaining redox balance and supporting the survival of breast cancer cells
Animal studies show robust activation of STING in heart, brain, and kidney after IR injury, and genetic or pharmacologic inhibition of STING reduces tissue damage and inflammation ( 2.1.2.4 Inflammasome-independent IL-33 and HMGB1 release Mitochondrial damage can also prompt stressed cells ( e.g