铁死亡在放射性肺炎中的作用机制及中西医干预研究进展

Ferroptosis in Radiation Pneumonitis: Mechanisms and Advances in Interventions Combining Traditional Chinese and Western Medicine

摘要: 放射性肺炎(Radiation Pneumonitis, RP)是胸部肿瘤放疗后常见的严重并发症，其发病机制复杂，涉及氧化应激、炎症反应及多种细胞死亡形式。近年来，铁死亡作为一种铁依赖性的非凋亡细胞死亡形式，在放射性肺炎的发生发展中受到广泛关注。现有研究表明，放疗诱导的活性氧爆发可导致铁代谢紊乱、脂质过氧化物堆积及谷胱甘肽过氧化物酶4 (GPX4)失活，进而触发肺部细胞铁死亡，促进炎症级联反应和肺纤维化进程。然而，现有研究多集中于单一机制或药物干预，缺乏对铁死亡调控网络的系统整合。本综述系统论述铁死亡在放射性肺炎中的分子机制并总结中西医干预的最新进展，旨在为临床防治提供新思路。

Abstract: Radiation pneumonitis is a common and serious complication following radiotherapy for thoracic tumors. Its pathogenesis is complex, involving oxidative stress, inflammatory responses and various forms of cell death. In recent years, ferroptosis—an iron-dependent form of non-apoptotic cell death—has attracted widespread attention in relation to the development of radiation pneumonitis. Existing research indicates that radiotherapy-induced bursts of reactive oxygen species can lead to iron metabolism disorders, the accumulation of lipid peroxides and the inactivation of glutathione peroxidase 4, thereby triggering ferroptosis in pulmonary cells and promoting inflammatory cascades and the progression of pulmonary fibrosis. However, existing studies have largely focused on single mechanisms or drug interventions, lacking a systematic integration of the ferroptosis regulatory network. This review systematically discusses the molecular mechanisms of ferroptosis in radiation pneumonitis and summarizes the latest advances in both Western and traditional Chinese medical interventions, aiming to provide new insights and targets for clinical prevention and treatment.