Wang Huimeng, Sun Jiajia, Luo Yongsheng, Li Xiaohu, Li Jinfeng
Department of Kidney Transplantation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Ren Fail. 2025 Dec;47(1):2536732. doi: 10.1080/0886022X.2025.2536732. Epub 2025 Aug 29.
Ferroptosis represents a distinctive mechanism of cell death, differing from necroptosis, necrosis, and apoptosis. It is triggered by the accumulation of lipid peroxides, driven by iron-catalyzed reactions. This oxidative damage is essential for triggering the ferroptotic pathway. Compared with apoptosis and necroptosis, ferroptosis is activated earlier in acute kidney injury (AKI), serving as a preemptive mechanism of cell death. Ferroptosis acts as a link between synchronous waves of renal tubular cell death by triggering cell death amplification loops and connects cell damage with inflammatory responses, thus constituting a crucial stage in the progression of AKI. This paper discusses the mechanisms that trigger ferroptosis in AKI and how ferroptosis, as a preemptive mode of cell death, exacerbates AKI through ferroptotic waves, modulates inflammatory responses, triggering apoptosis, necroptosis, and pyroptosis.
铁死亡代表一种独特的细胞死亡机制，不同于坏死性凋亡、坏死和凋亡。它由脂质过氧化物的积累引发，由铁催化反应驱动。这种氧化损伤对于触发铁死亡途径至关重要。与凋亡和坏死性凋亡相比，铁死亡在急性肾损伤（AKI）中更早被激活，作为一种先发的细胞死亡机制。铁死亡通过触发细胞死亡放大环，在肾小管细胞死亡的同步波之间起连接作用，并将细胞损伤与炎症反应联系起来，从而构成AKI进展中的关键阶段。本文讨论了在AKI中触发铁死亡的机制，以及铁死亡作为一种先发的细胞死亡模式，如何通过铁死亡波加剧AKI、调节炎症反应、触发凋亡、坏死性凋亡和焦亡。
