EPISODE · Dec 19, 2025 · 20 MIN
326-免疫代谢驱动线粒体过氧裂解
from 聊聊Sci
这篇文章介绍了由王等人发现的一种新的裂解性细胞死亡途径，命名为线粒体超氧化溶酶 (mitoxyperilysis)。这种死亡机制由先天免疫激活与代谢紊乱 (IIAMD)的协同作用触发，导致谷胱甘肽耗尽和线粒体产生氧化应激。在此过程中，受损的线粒体与细胞膜保持长时间接触，这一现象被称为线粒体超氧化损伤 (mitoxyperiosis)，最终引起细胞膜的局部氧化损伤并破裂。调节该过程的关键在于 mTORC2 信号通路，对该通路的抑制可以恢复细胞骨架活性，促使线粒体远离细胞膜以维持细胞完整性。这一机制区别于已知的细胞死亡模式（如凋亡或坏死），并具有重要的应用潜力，例如在小鼠模型中激活该通路可以减少肿瘤体积，为癌症和炎症性疾病提供了潜在的治疗靶点。References: Wang Y, Lu J, Carisey A F, et al. Innate immune and metabolic signals induce mitochondria-dependent membrane lysis via mitoxyperiosis[J]. Cell, 2025.前往小宇宙评论区与主播互动
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