The research field of regulated cell death is growing extensively. Following the recognition of ferroptosis, other unique and distinct forms of regulated cell death, including cuproptosis and disulfide death, have been identified. Disulfide death occurs due to the abnormal accumulation of disulfides within cells in environments lacking glucose, leading to contraction of the actin cytoskeleton, which ultimately triggers various signaling pathways and cell death. The induction of disulfide death in the treatment of cancer may exhibit significant therapeutic potential. Therefore, in the present review, a comprehensive and critical analysis of the current understanding of the molecular mechanisms and regulatory networks of disulfide death is presented. In addition, the potential physiological functions of disulfide death in tumor suppression and immune surveillance as well as its pathological roles and therapeutic potential are described. The core focus areas for future research into this form of cell death are also explored. Given the current lack of extensive clinical findings and well-defined key concepts, these may be regarded as pivotal points of interest in future studies.
Keywords: SLC7A11; disulfide death; glucose starvation; tumors.
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