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Regulatory mechanism of ferroptosis, a new mode of cell death

机译:铁减少症的调控机制,一种新的细胞死亡方式

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Ferroptosis is a newly discovered process of cell death that differs from apoptosis, autophagy, and pyroptosis. It is closely related to tumor formation, diseases that damage tissue, and neurodegenerative diseases. Activation of the extracellular regulated protein kinase (EPK) pathway and acylCOA synthetase long-chain family member 4 (ACSL4) are indicative of ferroptosis. During ferroptosis, the mitochondrial volume becomes smaller and the double membrane density increases. The process of ferroptosis involves disruption of the material redox reaction, and changes in the levels of cystine, glutathione, NADPH, and increase of GPX4, NOX, and ROS. Iron increases significantly in ferroptosis. Divalent iron ions can greatly promote lipid oxidation, ROS accumulation, and thus promote ferroptosis. The occurrence and progress of ferroptosis are influenced by multiple factors and signaling pathways.
机译:Ferroptosis是新发现的细胞死亡过程,不同于凋亡,自噬和发烧。它与肿瘤的形成,损害组织的疾病以及神经退行性疾病密切相关。细胞外调节蛋白激酶(EPK)途径和酰基COA合成酶长链家族成员4(ACSL4)的激活指示肥大症。在肥大症期间,线粒体体积变小,双膜密度增加。促铁作用过程涉及物质氧化还原反应的破坏,胱氨酸,谷胱甘肽,NADPH含量的变化以及GPX4,NOX和ROS的增加。铁在肥大症中显着增加。二价铁离子可以极大地促进脂质氧化,ROS积累,从而促进肥大化。受精卵的发生和发展受多种因素和信号通路的影响。

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