Lei Pengxu, Bai Tao, Sun Yuling
Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Zhengzhou University, School of Medicine, Institute of Hepatobiliary and Pancreatic Diseases, Zhengzhou University, Zhengzhou, China.
Front Physiol. 2019 Feb 26;10:139. doi: 10.3389/fphys.2019.00139. eCollection 2019.
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.
铁死亡是一种新发现的非凋亡性调节性细胞死亡(RCD)形式,其特征是脂质过氧化物的铁依赖性积累。它在形态和生化方面与已知的细胞死亡类型不同。铁死亡在肿瘤、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、半胱氨酸饥饿和花生四烯酰(AA)的过氧化会触发细胞中的铁死亡。铁螯合剂、亲脂性抗氧化剂和特异性抑制剂可预防铁死亡。尽管大量研究已经证明了铁死亡在人类中的重要性,但其机制尚不完全清楚。在本综述中,我们通过将铁死亡的机制分为两个方面来摆脱这种困惑:促进脂质过氧化物形成的过程和抑制脂质过氧化物还原的过程。同时,我们总结了铁死亡与几种细胞死亡类型之间的关系。