铁死亡在器官缺血再灌注损伤中的作用机制研究进展

缺血再灌注损伤（IRI）是导致器官功能障碍和移植失败的重要因素之一，其机制复杂，迄今未完全阐明，且缺乏有效治疗手段。IRI过程中，多种细胞死亡方式被激活，如凋亡、焦亡、自噬、程序性坏死等。铁死亡作为一种新型程序性细胞死亡方式，以铁依赖性的活性氧（ROS）自由基和脂质过氧化物堆积为主要特征，已被证实在IRI中发挥重要作用，通过调节铁、糖、氨基酸和脂质代谢及信号通路，加剧器官IRI。阻止铁死亡过程在多个器官中被证实能有效降低IRI的破坏，但与其他程序性细胞死亡方式相比，铁死亡在IRI中的作用机制研究仍较少。IRI与ROS产生密切相关，ROS通过诱发脂质过氧化反应，损害细胞膜结构，与铁死亡存在紧密联系。本文结合细胞铁死亡过程中的铁代谢、脂质过氧化、抗氧化系统及其他多种调节因子的调控途径，探讨铁死亡在器官IRI中扮演的多重角色，以期为IRI相关实验及临床治疗提供参考。

Research progress on the mechanism of ferroptosis in organ ischemia reperfusion injury

Ischemia-reperfusion injury (IRI) is one of the key factors leading to organ dysfunction and transplant failure. Its mechanism is complex and not yet fully elucidated, with limited treatment options. During IRI, various forms of cell death are activated, including apoptosis, pyroptosis, autophagy, and programmed necrosis. Ferroptosis, a novel form of programmed cell death characterized by iron-dependent reactive oxygen species (ROS) and lipid peroxidation accumulation, has been shown to play a significant role in IRI. By regulating iron, glucose, amino acid, and lipid metabolism, as well as signaling pathways, ferroptosis exacerbates organ IRI. Inhibiting ferroptosis has been proven to reduce IRI damage in multiple organs effectively, but compared to other forms of programmed cell death, the mechanisms of ferroptosis in IRI are still less studied. IRI is closely related to ROS production, which induces lipid peroxidation reactions and damages cell membrane structures, thereby being tightly linked to ferroptosis. This paper discusses the multifaceted roles of ferroptosis in organ IRI by examining the regulatory pathways of iron metabolism, lipid peroxidation, antioxidant systems, and other factors involved in cellular ferroptosis, aiming to provide references for IRI-related experiments and clinical treatments.