Ferroptosis, a form of regulated cell death, is initiated by oxidative perturbations of the intracellular microenvironment, which is under the constitutive control of glutathione peroxidase 4 (GPX4). Ferrous iron (Fe2+) accumulation and lipid peroxidation are critical events in the induction of ferroptosis, which is inhibited by iron chelators and lipophilic antioxidants. Ferroptosis terminates in mitochondrial dysfunction and toxic lipid peroxidation. It plays a vital role in inhibiting cancer growth and proliferation. It can be induced in cancer cells, and certain normal cells, by experimental compounds (e.g., erastin, Ras-selective lethal small molecule 3) or clinical drugs. The purpose of this review is to summarize the various drugs (e.g., sulfasalazine, lanperisone, sorafenib, fenugreek (trigonelline), acetaminophen, cisplatin, artesunate, combination of siramesine and lapatinib, ferumoxytol, and salinomycin (ironomycin)) that could induce ferroptosis in cancer cells and provide an overview of current knowledge regarding the mechanisms underlying ferroptosis. In future, we anticipate the development of more ferroptosis-inducing drugs, and the availability of such drugs for the clinical treatment of cancer.

中文翻译：

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Ferroptosis，一种抗癌药物的新药理机制。

受精症是一种受调节的细胞死亡形式，由谷胱甘肽过氧化物酶4（GPX4）的组成型控制下的细胞内微环境的氧化扰动引起。亚铁（Fe2 +）的积累和脂质过氧化是诱导铁定病的关键事件，受铁螯合剂和亲脂性抗氧化剂抑制。Ferroptosis以线粒体功能障碍和毒性脂质过氧化作用终止。它在抑制癌症的生长和扩散中起着至关重要的作用。它可以通过实验化合物（例如，Estinstin，Ras选择性致死小分子3）或临床药物在癌细胞和某些正常细胞中诱导。这篇综述的目的是总结各种药物（例如柳氮磺胺吡啶，兰培酮，索拉非尼，胡芦巴（trigonelline），对乙酰氨基酚，顺铂，青蒿琥酯，西拉美新与拉帕替尼，阿魏托仑和沙利霉素（伊罗霉素）的组合，可诱导癌细胞中的肥大症，并概述了有关肥大症潜在机制的最新知识。将来，我们预计会开发出更多的促肥大症的药物，并有望将这些药物用于临床治疗癌症。