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In further support of this model, glucose starvation-induced cell death and redox defects in SLC7A11 high cancer cells can be substantially blocked by treatments that restore NADPH levels and prevent cystine accumulation, such as treatment with 2DG (which inhibits glycolysis but can still be shunted into the PPP to generate NADPH) (Liu et al., 2020), suggesting that it is cystine accumulation and/or NADPH depletion resulting from cystine uptake that causes the cell death in SLC7A11 high cancer cells under glucose starvation

J Biol Chem 288:74677480 Sikiric P (1999) The pharmacological properties of the novel peptide BPC 157 (PL-10)

Empagliflozin effectively lowers liver fat content in well-controlled type 2 diabetes: a randomized, double-blind, phase 4, placebo-controlled trial

Intermittent hypoxia-hyperoxia training improves cognitive function and decreases circulating biomarkers of Alzheimers disease in patients with mild cognitive impairment: a pilot study

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