Zhang Han, Zhang Enxiang, Hu Hongbo
College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100080, China.
Key Laboratory of Growth Regulation and Transformation Research of Zhejiang Province, School of Life Sciences, Westlake Institute for Advanced Study, Westlake University, Hangzhou 310024, China.
Biomedicines. 2021 Nov 10;9(11):1660. doi: 10.3390/biomedicines9111660.
Non-alcoholic fatty liver disease (NAFLD) has become the chronic liver disease with the highest incidence throughout the world, but its pathogenesis has not been fully elucidated. Ferroptosis is a novel form of programmed cell death caused by iron-dependent lipid peroxidation. Abnormal iron metabolism, lipid peroxidation, and accumulation of polyunsaturated fatty acid phospholipids (PUFA-PLs) can all trigger ferroptosis. Emerging evidence indicates that ferroptosis plays a critical role in the pathological progression of NAFLD. Because the liver is the main organ for iron storage and lipid metabolism, ferroptosis is an ideal target for liver diseases. Inhibiting ferroptosis may become a new therapeutic strategy for the treatment of NAFLD. In this article, we describe the role of ferroptosis in the progression of NAFLD and its related mechanisms. This review will highlight further directions for the treatment of NAFLD and the selection of corresponding drugs that target ferroptosis.
非酒精性脂肪性肝病(NAFLD)已成为全球发病率最高的慢性肝病,但其发病机制尚未完全阐明。铁死亡是一种由铁依赖性脂质过氧化引起的新型程序性细胞死亡形式。铁代谢异常、脂质过氧化以及多不饱和脂肪酸磷脂(PUFA-PLs)的积累均可触发铁死亡。新出现的证据表明,铁死亡在NAFLD的病理进展中起关键作用。由于肝脏是铁储存和脂质代谢的主要器官,铁死亡是肝脏疾病的理想靶点。抑制铁死亡可能成为治疗NAFLD的一种新的治疗策略。在本文中,我们描述了铁死亡在NAFLD进展中的作用及其相关机制。本综述将重点介绍NAFLD治疗的进一步方向以及针对铁死亡的相应药物选择。