Department of Pharmaceutical Technology, NSHM Knowledge Campus, Kolkata-Group of Institutions, Kolkata, West Bengal, India.
Immunology. 2024 Aug;172(4):547-565. doi: 10.1111/imm.13789. Epub 2024 Apr 2.
Ferroptosis, a necrotic, iron-dependent controlled cell death mechanism, is distinguished by the development of lipid peroxides to fatal proportions. Malignant tumours, influenced by iron to promote fast development, are vulnerable to ferroptosis. Based upon mounting evidence it has been observed that ferroptosis may be immunogenic and hence may complement immunotherapies. A new approach includes iron oxide-loaded nano-vaccines (IONVs), having supremacy for the traits of the tumour microenvironment (TME) to deliver specific antigens through improving the immunostimulatory capacity by molecular disintegration and reversible covalent bonds that target the tumour cells and induce ferroptosis. Apart from IONVs, another newer approach to induce ferroptosis in tumour cells is through oncolytic virus (OVs). One such oncolytic virus is the Newcastle Disease Virus (NDV), which can only multiply in cancer cells through the p53-SLC7A11-GPX4 pathway that leads to elevated levels of lipid peroxide and intracellular reactive oxygen species leading to the induction of ferroptosis that induce ferritinophagy.
铁死亡是一种依赖于铁的坏死性、受调控的细胞死亡方式,其特征是脂质过氧化物的产生达到致命程度。受铁影响而促进快速发展的恶性肿瘤对铁死亡很敏感。有越来越多的证据表明,铁死亡可能具有免疫原性,因此可以补充免疫疗法。一种新的方法包括负载氧化铁的纳米疫苗(IONVs),它具有肿瘤微环境(TME)的优势,可以通过分子分解和针对肿瘤细胞的可逆共价键来提高免疫刺激能力,从而传递特定的抗原,诱导铁死亡。除了 IONVs,另一种诱导肿瘤细胞铁死亡的新方法是通过溶瘤病毒(OVs)。其中一种溶瘤病毒是新城疫病毒(NDV),它只能通过 p53-SLC7A11-GPX4 途径在癌细胞中复制,导致脂质过氧化物和细胞内活性氧水平升高,从而诱导铁死亡,进而诱导铁蛋白自噬。
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