SLC7A11 通过促进胱氨酸输入以增强谷胱甘肽合成并对抗氧化应激，在肿瘤发展中发挥关键作用。二硫下垂是一种在葡萄糖剥夺下高表达 SLC7A11 的细胞中观察到的一种新出现的细胞死亡形式，通过还原氧化反应和二硫键形成进行调节。这一过程导致质膜上的 F-肌动蛋白细胞骨架收缩和塌陷，最终导致细胞死亡。与其他形式的细胞死亡相比，二硫下垂表现出独特的特征和调节机制。这种机制为癌症治疗提供了新的见解和创新策略，同时也启发了其他疾病的潜在治疗方法。我们的综述重点是阐明二硫下垂的分子机制及其与肌动蛋白细胞骨架的联系，确定细胞死亡的替代代谢形式，并为基于二硫下垂的癌症治疗提供见解。对二硫下垂症的全面了解将有助于我们了解基本的细胞稳态，并促进疾病治疗的突破性疗法的开发。© 2024 作者。北京干细胞与再生医学研究院和John Wiley联合出版的《细胞增殖》

SLC7A11 plays a pivotal role in tumour development by facilitating cystine import to enhance glutathione synthesis and counteract oxidative stress. Disulphidptosis, an emerging form of cell death observed in cells with high expression of SLC7A11 under glucose deprivation, is regulated through reduction-oxidation reactions and disulphide bond formation. This process leads to contraction and collapse of the F-actin cytoskeleton from the plasma membrane, ultimately resulting in cellular demise. Compared to other forms of cell death, disulphidptosis exhibits distinctive characteristics and regulatory mechanisms. This mechanism provides novel insights and innovative strategies for cancer treatment while also inspiring potential therapeutic approaches for other diseases. Our review focuses on elucidating the molecular mechanism underlying disulphidptosis and its connection with the actin cytoskeleton, identifying alternative metabolic forms of cell death, as well as offering insights into disulphidptosis-based cancer therapy. A comprehensive understanding of disulphidptosis will contribute to our knowledge about fundamental cellular homeostasis and facilitate the development of groundbreaking therapies for disease treatment.© 2024 The Author(s). Cell Proliferation published by Beijing Institute for Stem Cell and Regenerative Medicine and John Wiley & Sons Ltd.