School of Clinical Medicine, Changchun University of Chinese Medicine, 130117 Changchun, Jilin, China.
State Key Laboratory of Electroanalytical Chemistry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, 130022 Changchun, Jilin, China.
Front Biosci (Landmark Ed). 2023 Dec 6;28(12):332. doi: 10.31083/j.fbl2812332.
Nonalcoholic fatty liver disease (NAFLD) constitutes a commonly diagnosed liver pathology with perturbed lipid metabolism, which is mainly caused by excessive accumulation of fat in hepatocytes by various pathogenic factors. Currently, there are no effective drug treatments for NAFLD. Ferroptosis represents a novel form of programmed cell death depending on iron, which is driven by large cellular amounts of reactive oxygen species (ROS) and lipid peroxides. Ferroptosis plays critical regulatory roles in the pathogenesis of NAFLD, and overaccumulation of Fe2+ contributes to lipid peroxidation, which subsequently aggravates NAFLD. Therefore, ferroptosis suppression might constitute an important target for NAFLD treatment. This article reviews the discovery, production pathways, and defense mechanisms of ferroptosis, and explores its association with NAFLD. This may provide new reference targets and strategies for the development of NAFLD drugs from the perspective of ferroptosis.
非酒精性脂肪性肝病（NAFLD）是一种常见的肝脏病理，其脂质代谢紊乱，主要由各种致病因素导致肝细胞内脂肪过度堆积引起。目前，NAFLD 尚无有效的药物治疗方法。铁死亡是一种新型的依赖于铁的程序性细胞死亡形式，由大量的活性氧（ROS）和脂质过氧化物驱动。铁死亡在 NAFLD 的发病机制中起着关键的调节作用，Fe2+ 的过度积累导致脂质过氧化，进而加重 NAFLD。因此，抑制铁死亡可能是治疗 NAFLD 的一个重要靶点。本文综述了铁死亡的发现、产生途径和防御机制，并探讨了其与 NAFLD 的关系。这可能为从铁死亡的角度开发 NAFLD 药物提供新的参考靶点和策略。
