铁死亡是一种依赖铁离子的程序性细胞死亡方式，其特征为脂质过氧化、氧化应激和铁代谢紊乱，在青光眼的发病过程中具有重要作用。文章系统综述了铁死亡的基本机制、青光眼中的氧化应激与铁死亡、铁死亡与青光眼神经退行性变的关系、铁死亡在青光眼治疗中的潜在策略。研究发现，铁死亡调控因子在缓解氧化损伤、维持细胞功能方面发挥着关键作用。然而其调控机制的复杂性不仅限制了对其作用的深入理解，也阻碍了相关成果的临床转化。尽管铁死亡抑制剂在动物模型中表现出良好的视神经保护效应，但其在临床应用中亦面临药物安全性和靶向特异性等问题。未来需开发更具靶向性、低毒性的干预策略，以推动青光眼的个体化精准治疗。

Ferroptosis, an iron-dependent form of programmed cell death characterized by lipid peroxidation, oxidative stress, and dysregulated iron metabolism, plays a significant role in the pathogenesis of glaucoma. This review systematically summarizes the fundamental mechanisms of ferroptosis, the involvement of oxidative stress and ferroptosis in glaucoma, the relationship between ferroptosis and glaucomatous neurodegeneration, and the potential therapeutic strategies targeting ferroptosis in glaucoma. Studies have shown that ferroptosis-regulating factors play a crucial role in mitigating oxidative damage and preserving cellular function. However, the complexity of their regulatory mechanisms not only hinders a comprehensive understanding of their roles but also impedes clinical translation. Although ferroptosis inhibitors have demonstrated promising neuroprotective effects in animal models, their clinical application remains challenged by issues such as drug safety and target specificity. Therefore, the development of more targeted and low-toxicity therapeutic strategies is essential to advance personalized and precise treatment for glaucoma.

国家自然科学基金项目(No.82060179,82460207); 广西重点研发计划项目(No.桂科AB24010171); 广西卫健委自筹课题项目(No.Z20200830)