放射增敏剂
抗辐射性
GPX4
程序性细胞死亡
癌症研究
脂质过氧化
LNCaP公司
化学
放射治疗
诱导剂
癌细胞
癌症
生物化学
医学
氧化应激
内科学
细胞凋亡
谷胱甘肽过氧化物酶
超氧化物歧化酶
基因
作者
Fatemeh-Jalali Zefrei,Mohammd Shormij,Leila Dastranj,Maryam Alvandi,Zahra Shaghaghi,Soghra Farzipour,Nasim Zarei-Polgardani
出处
期刊:Current Radiopharmaceuticals
[Bentham Science]
日期:2023-11-17
卷期号:17 (1): 14-29
标识
DOI:10.2174/0118744710262369231110065230
摘要
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.
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