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首页> 外文期刊>Chemico-biological interactions >Functional role of ferroptosis on cancers, activation and deactivation by various therapeutic candidates-an update
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Functional role of ferroptosis on cancers, activation and deactivation by various therapeutic candidates-an update

机译:裂解病的功能作用对各种治疗候选者的癌症,激活和失活的作用 - 更新

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摘要

Ferroptosis is recently identified form of regulated cell death which differs from previously identified cell death in a way that it is driven by iron-dependent lipid peroxide accumulation. Morphologically, cell volume shrinkage and increased mitochondrial membrane density are main features which characterize this form of cell death. Molecular mechanism of ferroptosis induction involved suppression of the phospholipid glutathione peroxidase 4 (GPX4) and further intracellular accumulation of lipid reactive oxygen species (ROS), a process in which iron is involved; either via inhibition of system Xc- (cystine/glutamate antiporter) or direct inhibition of GPX4. Several other pathways like RAS/MAPK and NRF2 are found to be involved in ferroptosis regulation. However, the precise mechanism of ferroptosis induction is not revealed till date. Like other regulated cell deaths, ferroptosis plays important role in tumor suppression and progression as revealed by several scientific reports. This review summarizes basic information about discovery of this novel cell death mechanism including molecular mechanism of its induction and further explains the roles of ferroptosis in human cancers.
机译:最近鉴定了枯枝叶蛋白的规定细胞死亡的形式,其不同于先前鉴定的细胞死亡,以至于它是由铁依赖性脂质过氧化物积累的驱动的方式。形态学上,细胞体积收缩和增加的线粒体膜密度是表征这种形式的细胞死亡的主要特征。脱盐诱导的分子机制涉及抑制磷脂谷胱甘肽过氧化物酶4(GPX4)和进一步的脂质活性氧(ROS)的细胞内积累,涉及铁的方法;通过抑制系统XC-(胱氨酸/谷氨酸酯酸)或直接抑制GPX4。发现RAS / MAPK和NRF2等其他几种途径参与了硬化调节。然而,迄今为止,不揭示脱叶菌诱导的精确机制。与其他受管制的细胞死亡一样,脱裂病症在肿瘤抑制和进展中起着重要作用,如几个科学报告所揭示的。本综述总结了有关发现这种新细胞死亡机制的基本信息,包括其诱导的分子机制,进一步解释了硬化在人类癌症中的角色。

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