Department of Gastroenterology, Research Institute of Digestive Diseases, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Queen Mary College of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Mol Med Rep. 2021 Mar;23(3). doi: 10.3892/mmr.2021.11864. Epub 2021 Jan 26.
Ischemia‑reperfusion injury (IRI), also called reoxygenation injury, is the outcome of inflammatory processes and oxidative damage through the induction of oxidative stress. In the clinical setting, IRI contributes to severe hepatic injury, including liver cell death by apoptosis and ferroptosis. Ferroptosis is a novel type of cell death in hepatic IRI that involves small molecules that inhibit glutathione biosynthesis or glutathione peroxidase 4 (GPX4), which is a glutathione‑dependent antioxidant enzyme, causing mitochondrial damage. Currently, ferroptosis has been systematically described in neurological settings, kidney diseases and different types of cancer, while few studies have analysed the presence of ferroptosis and the regulatory mechanism of ferroptosis in hepatic IRI. Exploring the exact role played by ferroptosis in the liver following hepatic IRI in accordance with existing evidence and mechanisms could guide potential therapeutic interventions and provide a novel research avenue.
缺血再灌注损伤（IRI），也称为再氧化损伤，是炎症过程和氧化损伤通过诱导氧化应激的结果。在临床环境中，IRI 导致严重的肝损伤，包括细胞凋亡和铁死亡导致的肝细胞死亡。铁死亡是一种新的细胞死亡类型，涉及抑制谷胱甘肽生物合成或谷胱甘肽过氧化物酶 4（GPX4）的小分子，GPX4 是一种谷胱甘肽依赖的抗氧化酶，导致线粒体损伤。目前，铁死亡已在神经系统疾病、肾脏疾病和不同类型的癌症中得到系统描述，而很少有研究分析铁死亡的存在及其在肝 IRI 中的调控机制。根据现有证据和机制，探索铁死亡在肝 IRI 后肝脏中的确切作用可能指导潜在的治疗干预，并提供新的研究途径。
