撰文丨王聪 编辑丨王多鱼 排版丨水成文 2020 年， 张义 团队 研究团队从感染性心内膜炎患者体内分离出一株 Bergeyella cardium 突变株 （BCV） 。与原始菌株相比，BCV 表现出更强的血清抗性和 致病能力。 在这项最新研究中，研究团队发现， BCV 可诱导 巨噬细胞 产生独特的胞质空泡化细胞死亡和轻微的凋亡样细胞死亡，研究团队将这种细胞死亡方式命名为—— Floatptosis ，这一细胞死亡过程以溶酶体融合相关终止 （ F used L ysosome- a ssociated t ermination ） 为特征，且可被钠通道抑制剂 阿米洛利 特异性抑 制。 实验证实，BCV 分泌的外膜囊泡 （OMV） 或其携带的桶状膜蛋白成分 （包括脂质运载蛋白、β-桶状结构及PorV蛋白） ，通过转染方式足以显著诱导胞质空泡 化表型。分子机制研究显示， SLC9A9 通过促进空泡融合，在 BCV 感染、OMV 及桶状蛋白触发的空泡化死亡通路中发挥关键调控作用。 细菌病原体已进化出多种机制来调控宿主细胞死亡、逃逸宿主免疫并建立持续性感染。 2025 年 10 月 21 日， 山东大学 高等医学研 ...

Core Viewpoint - Ferroptosis is a novel form of programmed cell death characterized by abnormal accumulation of iron ions and explosive generation of reactive oxygen species (ROS), leading to lipid peroxidation of cell membranes. Recent studies indicate its association with various diseases, including cancer and neurodegenerative disorders, making it a potential therapeutic target [2]. Group 1 - N-acetyl-L-cysteine (NAC) is widely recognized as an antioxidant in cell death research and is increasingly acknowledged for its role in inhibiting ferroptosis [2][5]. - The research team led by Professor Marcus Conrad published findings that NAC treatment can rapidly replenish intracellular cysteine pools, enhancing its function as a cysteine precursor [6]. - The study revealed that both NAC and its enantiomer D-NAC can act as direct reducing substrates for glutathione peroxidase 4 (GPX4), combating lipid peroxidation independently of glutathione synthesis [6][7]. Group 2 - The core findings of the study include that NAC and D-NAC can inhibit ferroptosis independently of cellular glutathione (GSH) [7]. - The presence of GPX4 is essential for NAC and D-NAC to exert their inhibitory effects on ferroptosis [7]. - GPX4 can utilize various reducing substrates to reduce lipid hydroperoxides, indicating a broader role for GPX4 in ferroptosis regulation [9].