心磷脂
串扰
细胞色素c
细胞凋亡
线粒体
脂质过氧化
程序性细胞死亡
化学
线粒体内膜
细胞生物学
生物物理学
线粒体通透性转换孔
膜
生物
氧化应激
生物化学
物理
光学
磷脂
作者
Jinping Tang,Jinyu Zhu,Han Xie,Song Li,Guangyang Xu,Wei Li,Linjun Cai,Xiao Han
出处
期刊:Nano Letters
[American Chemical Society]
日期:2024-02-11
卷期号:24 (7): 2384-2391
标识
DOI:10.1021/acs.nanolett.3c05039
摘要
Ferroptosis and apoptosis are two types of regulated cell death that are closely associated with the pathophysiological processes of many diseases. The significance of ferroptosis–apoptosis crosstalk in cell fate determination has been reported, but the underlying molecular mechanisms are poorly understood. Herein mitochondria-mediated molecular crosstalk is explored. Based on a comprehensive spectroscopic investigation and mass spectrometry, cytochrome c-involved Fenton-like reactions and lipid peroxidation are revealed. More importantly, cytochrome c is found to induce ROS-independent and cardiolipin-specific lipid peroxidation depending on its redox state. In situ Raman spectroscopy unveiled that erastin can interrupt membrane permeability, specifically through cardiolipin, facilitating cytochrome c release from the mitochondria. Details of the erastin–cardiolipin interaction are determined using molecular dynamics simulations. This study provides novel insights into how molecular crosstalk occurs around mitochondrial membranes to trigger ferroptosis and apoptosis, with significant implications for the rational design of mitochondria-targeted cell death reducers in cancer therapy.
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