谷胱甘肽
线粒体通透性转换孔
细胞生物学
活性氧
程序性细胞死亡
信号转导
线粒体
细胞凋亡
氧化应激
生物
转录因子
线粒体ROS
生物能学
细胞信号
化学
生物化学
酶
基因
作者
Liyun Yuan,Neil Kaplowitz
标识
DOI:10.1016/j.mam.2008.08.003
摘要
Glutathione (GSH) is a major antioxidant as well as redox and cell signaling regulator. GSH guards cells against oxidative injury by reducing H2O2 and scavenging reactive oxygen and nitrogen radicals. In addition, GSH-induced redox shift with or without ROS subjects some cellular proteins to varied forms of oxidation, altering the function of signal transduction and transcription factor molecules. Increasing evidence supports the important role of ROS and GSH in modulating multiple signaling pathways. TNF-α and Fas signaling, NF-κB, JNK and mitochondrial apoptotic pathways are the focus of this review. The redox regulation either can switch on/off or regulate the threshold for some crucial events in these pathways. Notably, mitochondrial GSH depletion induces increased mitochondrial ROS exposure which impairs bioenergetics and promotes mitochondrial permeability transition pore opening which is critical for cell death. Depending on the extent of mitochondrial damage, NF-κB inhibition and JNK activation, hepatocytes may either undergo different modes of cell death (apoptosis or necrosis) or be sensitized to cell-death stimuli (i.e. TNF-α). These processes have been implicated in the pathogenesis of many liver diseases.
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