摘要无机砷是存在于环境中的致癌物。肝脏作为砷代谢的主要靶器官，长期接触无机砷，可通过肝纤维化、肝硬化两个阶段最终导致癌变。铁死亡是铁依赖性脂质过氧化物大量积聚，影响线粒体正常功能而引起细胞程序性死亡的方式。研究发现，肝纤维化过程中存在铁死亡。长期以来，无机砷致肝纤维化一直是全球性的健康问题，但目前为止尚缺乏有效的治疗手段，铁死亡的发现为这一问题的研究提供了新思路。因此，本文将对无机砷致肝损伤及铁死亡机制研究的进展做一综述。

abstractsInorganic arsenic (iAs) is a common carcinogen that exists in the environment. Liver, as the main target organ of arsenic metabolism, long-term exposure to iAs can ultimately lead to carcinogenesis through two stages: liver fibrosis and cirrhosis. Ferroptosis is a type of programmed cell death caused by the accumulation of iron dependent lipid peroxides that affects the normal function of mitochondria. It has been found that ferroptosis occurs during liver fibrosis. Liver fibrosis caused by iAs has been a global health problem for a long time, but so far there is no effective treatment. The discovery of ferroptosis provides a new way to solve this problem. Therefore, this article will review the research progress of the mechanism of liver injury caused by iAs and ferroptosis.