Figure 2.

Molecular mechanisms of disulfidptosis. The study found that under glucose starvation, excessive consumption of reduced coenzyme II (NADPH) in tumour cells leads to abnormal accumulation of disulfides such as cystine, inducing disulfide stress, which triggers actin cytoskeleton contraction and cell death. Furthermore, cystine uptake is primarily mediated by the solute carrier family member SLC7A11 on the cell membrane. High expression of SLC7A11 significantly accelerates disulfidptosis in tumour cells under glucose starvation. (Glu: glucose; PPP: Pentose Phosphate Pathway; R5P: Ribose-5-phosphate; WRC: WAVE Regulatory Complex) (Figure created using Figdraw).