在慢性肝病发展过程中，肝脏可能会遭受氧化损伤。尽管过量的活性氧/氮物质（ROS/RNS）在病理条件下对肝脏所有组成部分都有害，但它们在肝脏稳态中的生理相关性不可忽视。慢性氧化应激和持续的炎症导致了纤维化调节星状细胞（HSCs）的活化以及后续的肝纤维化、肝硬化和肝癌病理过程。肝脏抗氧化和修复系统，以及自噬和铁死亡机制，参与了疾病发展的起始和轨迹。本综述讨论了不同原因引起的肝纤维化的ROS/RNS相关机制，并重点介绍了以修复肝细胞中的氧化/亚硝化应激或靶向HSC激活为前提的抗纤维化疗法的临床前和临床试验。版权所有 © 2023 Elsevier Ltd. 发表。

The liver can succumb to oxidant damage during the development of chronic liver diseases. Despite their physiological relevance to hepatic homeostasis, excessive reactive oxygen/nitrogen species (ROS/RNS) production under pathological conditions is detrimental to all liver constituents. Chronic oxidative stress coupled to unresolved inflammation sets in motion the activation of profibrogenic hepatic stellate cells (HSCs) and later pathogenesis of liver fibrosis, cirrhosis, and liver cancer. The liver antioxidant and repair systems, along with autophagic and ferroptotic machineries, are implicated in the onset and trajectory of disease development. In this review, we discuss the ROS/RNS-related mechanisms underlying liver fibrosis of distinct etiologies and highlight preclinical and clinical trials of antifibrotic therapies premised on remediating oxidative/nitrosative stress in hepatocytes or targeting HSC activation.Copyright © 2023. Published by Elsevier Ltd.