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Disulfidptosis is a newly identified form of regulated cell death driven by high SLC7A11 expression under glucose starvation. Mechanistically, massive cystine influx via SLC7A11, coupled with NADPH depletion due to glucose deprivation, leads to cystine accumulation, disulfide stress, aberrant crosslinking of actin cytoskeleton (notably at Cys257, Cys284, and Cys373), and eventual membrane rupture. This process is independent of apoptosis, ferroptosis, and necroptosis. This review systematically outlines the molecular regulatory network of disulfidptosis, including upstream triggers, key execution molecules (glutathione and thioredoxin systems, RAC1/WRC/Arp2/3 axis), and downstream effectors. We further evaluate its therapeutic potential across various malignancies (glioblastoma, hepatocellular, gastric, colorectal, pancreatic, breast, lung, and prostate cancers) and other diseases (neurodegenerative, metabolic, orthopedic, cardiovascular). Recent advances in nanodelivery systems for selective disulfidptosis induction are summarized. Key translational challenges are critically analyzed, including targeting specificity, safety, delivery barriers, resistance mechanisms, and biomarker deficiency. By exploiting metabolic vulnerabilities (high SLC7A11 expression and glucose dependence) of pathological cells, disulfidptosis opens a new therapeutic window that can synergize with ferroptosis, cuproptosis, and immunotherapy. This review provides a comprehensive framework for basic research and clinical translation of disulfidptosis-targeted therapies.