Ferroptosis Inducers as Promising Radiosensitizer Agents in Cancer Radiotherapy.

IF 1.5 4区 医学 Q3 PHARMACOLOGY & PHARMACY
Fatemeh-Jalali Zefrei, Mohammd Shormij, Leila Dastranj, Maryam Alvandi, Zahra Shaghaghi, Soghra Farzipour, Nasim Zarei-Polgardani
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引用次数: 0

Abstract

Radiotherapy (RT) failure has historically been mostly attributed to radioresistance. Ferroptosis is a type of controlled cell death that depends on iron and is caused by polyunsaturated fatty acid peroxidative damage. Utilizing a ferroptosis inducer may be a successful tactic for preventing tumor growth and radiotherapy-induced cell death. A regulated form of cell death known as ferroptosis is caused by the peroxidation of phospholipids containing polyunsaturated fatty acids in an iron-dependent manner (PUFA-PLs). The ferroptosis pathway has a number of important regulators. By regulating the formation of PUFA-PLs, the important lipid metabolism enzyme ACSL4 promotes ferroptosis, whereas SLC7A11 and (glutathione peroxidase 4) GPX4 prevent ferroptosis. In addition to introducing the ferroptosis inducer chemicals that have recently been demonstrated to have a radiosensitizer effect, this review highlights the function and methods by which ferroptosis contributes to RT-induced cell death and tumor suppression in vitro and in vivo.

铁下垂诱导剂在癌症放射治疗中的应用前景。
放射治疗(RT)失败历来主要归因于放射耐药。铁死亡是一种依赖于铁的受控细胞死亡,是由多不饱和脂肪酸过氧化损伤引起的。利用铁下垂诱导剂可能是一种成功的策略,以防止肿瘤生长和放疗诱导的细胞死亡。一种被称为铁凋亡的细胞死亡的调节形式是由含多不饱和脂肪酸的磷脂以铁依赖的方式过氧化引起的(PUFA-PLs)。铁下垂途径有许多重要的调节因子。通过调节PUFA-PLs的形成,重要的脂质代谢酶ACSL4促进铁下垂,而SLC7A11和(谷胱甘肽过氧化物酶4)GPX4则阻止铁下垂。除了介绍最近被证明具有放射增敏作用的铁下垂诱导剂化学物质外,本文还重点介绍了铁下垂在体外和体内促进rt诱导的细胞死亡和肿瘤抑制的功能和方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Current radiopharmaceuticals
Current radiopharmaceuticals PHARMACOLOGY & PHARMACY-
CiteScore
3.20
自引率
4.30%
发文量
43
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