Abstract：
Disulfidptosis is a novel form of cell death that is distinguishable from established programmed cell death pathways such as apoptosis, pyroptosis, autophagy, ferroptosis, and oxeiptosis. This process is characterized by the rapid depletion of nicotinamide adenine dinucleotide phosphate (NADPH) in cells and high expression of solute carrier family 7 member 11 (SLC7A11) during glucose starvation, resulting in abnormal cystine accumulation, which subsequently induces andabnormal disulfide bond formation in actin cytoskeleton proteins, culminating in actin network collapse and disulfidptosis. This review aimed to summarize the underlying mechanisms, influencing factors, comparisons with traditional cell death pathways, associations with related diseases, application prospects, and future research directions related to disulfidptosis.
摘要：
二硫键凋亡是一种新的细胞死亡形式，与已建立的程序性细胞死亡途径如细胞凋亡有区别。焦亡,自噬,铁性凋亡,和下垂。该过程的特征是在葡萄糖饥饿期间，细胞中烟酰胺腺嘌呤二核苷酸磷酸（NADPH）的快速消耗和溶质载体家族7成员11（SLC7A11）的高表达，导致胱氨酸异常积累，随后在肌动蛋白细胞骨架蛋白中诱导和异常的二硫键形成，最终导致肌动蛋白网络崩溃和二硫化物下垂。这篇综述旨在总结潜在的机制，影响因素，与传统细胞死亡途径的比较，与相关疾病的关联，应用前景,和未来的研究方向。
