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Mechanisms of Ferroptosis and Relations With Regulated Cell Death: A Review

机译:肥大症的发病机制及其与细胞死亡调控的关系

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摘要

Ferroptosis is a newly identified form of nonapoptotic regulated cell death (RCD) characterized by iron-dependent accumulation of lipid peroxides. It is morphologically and biochemically different from known types of cell death. Ferroptosis plays a vital role in the treatment of tumors, renal failure, and ischemia reperfusion injury (IRI). Inhibition of glutathione peroxidase 4 (GPX4), starvation of cysteine, and peroxidation of arachidonoyl (AA) trigger ferroptosis in the cells. Iron chelators, lipophilic antioxidants, and specific inhibitor prevent ferroptosis. Although massive researches have demonstrated the importance of ferroptosis in human, its mechanism is not really clear. In this review, we distanced ourselves from this confusion by dividing the mechanisms of ferroptosis into two aspects: processes that facilitate the formation of lipid peroxides and processes that suppress the reduction of lipid peroxides. At the same time, we summarize the relations between ferroptosis and several types of cell death.
机译:Ferroptosis是一种新发现的非凋亡调节型细胞死亡(RCD)形式,其特征是脂质过氧化物的铁依赖性积累。在形态和生化上与已知的细胞死亡类型不同。 Ferroptosis在肿瘤,肾衰竭和缺血再灌注损伤(IRI)的治疗中起着至关重要的作用。谷胱甘肽过氧化物酶4(GPX4)的抑制,半胱氨酸的饥饿和花生四烯酰(AA)的过氧化会触发细胞中的肥大病。铁螯合剂,亲脂性抗氧化剂和特定抑制剂可预防铁锈病。尽管大量研究证明了肥大症在人类中的重要性,但其机制尚不清楚。在这篇综述中,我们通过将肥大症的发病机制分为两个方面来避免这种困惑:促进脂质过氧化物形成的过程和抑制脂质过氧化物减少的过程。同时,我们总结了肥大症与几种类型的细胞死亡之间的关系。

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