Cardiovascular Diseases Research Center, Department of Cardiology, Heshmat Hospital, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran.
Pharmacology and Toxicology Department, Faculty of Pharmacy and Pharmaceutical Sciences-Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Curr Radiopharm. 2024;17(1):14-29. doi: 10.2174/0118744710262369231110065230.
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 and .
放疗失败在历史上主要归因于放射抵抗。铁死亡是一种依赖于铁的受控细胞死亡类型,由多不饱和脂肪酸过氧化损伤引起。利用铁死亡诱导剂可能是预防肿瘤生长和放疗诱导细胞死亡的成功策略。铁死亡是一种受调控的细胞死亡形式,是由铁依赖性多不饱和脂肪酸磷脂(PUFA-PLs)的过氧化引起的。铁死亡途径有许多重要的调节剂。通过调节 PUFA-PLs 的形成,重要的脂质代谢酶 ACSL4 促进铁死亡,而 SLC7A11 和(谷胱甘肽过氧化物酶 4)GPX4 则阻止铁死亡。除了介绍最近被证明具有放射增敏作用的铁死亡诱导剂化学物质外,本综述还强调了铁死亡在放疗诱导细胞死亡和肿瘤抑制中的作用和方法。