卵巢癌(OC),以其杀伤力和对化疗的抵抗力而闻名,与铁代谢和铁死亡密切相关-铁依赖的细胞死亡过程,有别于自噬和凋亡。新出现的证据表明,铁代谢的失调可能通过诱导氧化还原系统的失衡在OC中起关键作用,这导致了铁性凋亡,提供了一种新的治疗方法。这篇综述探讨了铁代谢的中断,影响氧化还原平衡,影响OC进展,专注于其基本的细胞功能和作为治疗靶标的潜力。它突出了分子的相互作用,包括非编码RNA(ncRNAs)的作用,在铁代谢和铁死亡之间,探索它们与关键免疫细胞如巨噬细胞和T细胞的相互作用,以及肿瘤微环境中的炎症。该综述还讨论了糖酵解相关的铁代谢如何通过活性氧物种影响铁凋亡。瞄准这些途径,特别是通过调节铁代谢和铁凋亡的药物,提出了有希望的治疗前景。该综述强调需要更深入地了解氧化还原调节系统中的铁代谢和铁死亡,以增强OC治疗,并主张继续研究这些机制作为对抗OC的潜在策略。
Ovarian cancer (OC), known for its lethality and resistance to chemotherapy, is closely associated with iron metabolism and ferroptosis-an iron-dependent cell death process, distinct from both autophagy and apoptosis. Emerging evidence suggests that dysregulation of iron metabolism could play a crucial role in OC by inducing an imbalance in the redox system, which leads to ferroptosis, offering a novel therapeutic approach. This review examines how disruptions in iron metabolism, which affect redox balance, impact OC progression, focusing on its essential cellular functions and potential as a therapeutic target. It highlights the molecular interplay, including the role of non-coding RNAs (ncRNAs), between iron metabolism and ferroptosis, and explores their interactions with key immune cells such as macrophages and T cells, as well as inflammation within the tumor microenvironment. The review also discusses how glycolysis-related iron metabolism influences ferroptosis via reactive oxygen species. Targeting these pathways, especially through agents that modulate iron metabolism and ferroptosis, presents promising therapeutic prospects. The review emphasizes the need for deeper insights into iron metabolism and ferroptosis within the redox-regulated system to enhance OC therapy and advocates for continued research into these mechanisms as potential strategies to combat OC.