Research status and molecular mechanisms of disulfidptosis in cardiovascular diseases (Review)

Figures

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  Figure 1.. Disulfidptosis mechanism. The cystine transporter SLC7A11 imports extracellular cystine. Under glucose-sufficient conditions, NADPH produced via the PPP and glycolysis-tricarboxylic acid cycle coupling supports cystine reduction to cysteine. Glucose deprivation suppresses PPP activity, depleting NADPH, halting cystine reduction and leading to cystine accumulation. The resulting disulfide stress causes spontaneous oxidation of free sulfhydryl groups on F-actin, forming aberrant intra- and intermolecular disulfide bonds. This crosslinking disrupts the actin cytoskeleton, ultimately triggering cell death. The WRC and Rac1 GTPase accelerate disulfidptosis by promoting lamellipodia formation, which provides additional actin networks for disulfide crosslinking in SLC7A11-upregulated cells. G6P, glucose 6-phosphate; 6PG, 6-phosphogluconate; R5P, ribose 5-phosphate; WRC, WAVE regulatory complex; SLC7A11, solute carrier family 7 member 11; F-actin, filamentous actin; NADPH, nicotinamide adenine dinucleotide phosphate; PPP, pentose phosphate pathway.

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  Figure 2.. Disulfidptosis in the cardiovascular system.