Posttranslational Modifications in Ferroptosis.

Posttranslational Modifications in Ferroptosis.
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铁死亡中的翻译后修饰

DOI:
10.1155/2020/8832043
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发表时间:
2020
影响因子:
--
通讯作者:
Jiang DS
Jiang DS
中科院分区:
生物学2区
文献类型:
--
作者:
Wei X;Yi X;Zhu XH;Jiang DS

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铁凋亡(Ferroptosis)于2012年首次提出,描述了以铁依赖性脂质过氧化为特征的调节性细胞死亡(RCD)形式。迄今为止,铁凋亡已经涉及许多疾病,例如癌发生、退行性疾病(例如,亨廷顿氏病、阿尔茨海默氏病和帕金森氏病)、缺血-再灌注损伤和心血管疾病。以前的研究已经确定了许多涉及铁凋亡的靶点;例如,酰基辅酶A合成酶长链家族成员4(ACSL 4)和p53诱导,而谷胱甘肽过氧化物酶4(GPX 4)和谷胱甘肽诱导因子α相关2(AIFM 2,也称为FSP 1)抑制铁凋亡。至少有三种主要途径(谷胱甘肽-GPX 4、FSP 1-辅酶Q10(CoQ 10)和GTP环化水解酶-1-(GCH 1-)四氢生物蝶呤(BH 4)途径)已被确定参与铁凋亡调节。最近的进展也强调了蛋白质的翻译后修饰(PTM)在铁凋亡中的重要作用。在这里,我们总结了最近发现的有关铁凋亡的机制,特别是在铁凋亡调控的PTM的作用的知识。
Ferroptosis was first coined in 2012 to describe the form of regulated cell death (RCD) characterized by iron-dependent lipid peroxidation. To date, ferroptosis has been implicated in many diseases, such as carcinogenesis, degenerative diseases (e.g., Huntington's, Alzheimer's, and Parkinson's diseases), ischemia-reperfusion injury, and cardiovascular diseases. Previous studies have identified numerous targets involved in ferroptosis; for example, acyl-CoA synthetase long-chain family member 4 (ACSL4) and p53 induce while glutathione peroxidase 4 (GPX4) and apoptosis-inducing factor mitochondria-associated 2 (AIFM2, also known as FSP1) inhibit ferroptosis. At least three major pathways (the glutathione-GPX4, FSP1-coenzyme Q10 (CoQ10), and GTP cyclohydrolase-1- (GCH1-) tetrahydrobiopterin (BH4) pathways) have been identified to participate in ferroptosis regulation. Recent advances have also highlighted the crucial roles of posttranslational modifications (PTMs) of proteins in ferroptosis. Here, we summarize the recently discovered knowledge regarding the mechanisms underlying ferroptosis, particularly the roles of PTMs in ferroptosis regulation.
ACSL4 通过塑造细胞脂质成分来决定铁死亡敏感性。
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