双硫死亡的分子机制、疾病关联及治疗应用 研究综述

Review on the Molecular Mechanism, Disease Association and Therapeutic Application of Disulfidptosis

摘要: 双硫死亡(disulfidptosis)是2023年被发现的新型程序性细胞死亡方式，其核心特征为二硫键异常积累引发的细胞骨架破坏，与传统凋亡、铁死亡等细胞死亡途径存在显著差异。该过程依赖溶质载体家族7成员11 (SLC7A11)高表达，在葡萄糖匮乏或氧化应激条件下，通过耗竭还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)、诱发二硫化物应激，最终导致肌动蛋白骨架崩溃而实现细胞死亡。近年来，双硫死亡在缺血性脑卒中、肿瘤等疾病中的作用机制及调控网络逐渐被揭示，为疾病的精准治疗提供了新视角。本文系统综述双硫死亡的分子机制、与疾病的关联、调控策略及研究展望，旨在整合当前研究进展，为相关领域的深入探索提供参考。

Abstract: Disulfidptosis is a novel type of programmed cell death discovered in 2023. Its core feature is cytoskeletal disruption caused by the aberrant accumulation of disulfide bonds, which is significantly different from traditional cell death pathways, such as apoptosis and ferroptosis. This process relies on the high expression of solute carrier family 7 member 11 (SLC7A11). Under glucose deprivation or oxidative stress, it depletes nicotinamide adenine dinucleotide phosphate (NADPH) and induces disulfide stress, ultimately leading to the collapse of the actin cytoskeleton and cell death. In recent years, the mechanisms and regulatory networks of disulfidptosis in diseases including ischemic stroke and tumors have been gradually revealed, providing a new perspective for the precision therapy of diseases. This paper systematically reviews the molecular mechanisms of disulfidptosis, its association with diseases, regulatory strategies and research prospects. It aims to integrate the current research progress and provide a reference for further exploration in related fields.