文献类型：期刊文献

英文题名：Reappraising heme oxygenase-1 as a ferroptosis modulator in atherosclerosis: a mechanism-focused review

作者：Xu, Jia[1];Chen, Che[1];Yuan, Han-Ying[1];Zhang, You-Yu[2];Wang, Chang-Rong[1,3];Xi, Xuan[1];Pan, Heng[1];Li, De-Hong[4];Lu, Yan[5]

第一作者：徐婧

通信作者：Lu, Y[1]

机构：[1]Gansu Univ Chinese Med, Sch Publ Hlth, Lanzhou, Gansu, Peoples R China;[2]Fudan Univ, Sch Clin Med, Shanghai, Peoples R China;[3]944 Hosp Joint Logist Support Force, Dept Lab & Blood Transfus, Jiuquan, Gansu, Peoples R China;[4]Gansu Prov Hosp, Dept Blood Transfus, Lanzhou, Gansu, Peoples R China;[5]Gansu Prov Hosp, Dept Clin Lab, Lanzhou, Gansu, Peoples R China

第一机构：甘肃中医药大学公共卫生学院

通信机构：[1]corresponding author), Gansu Prov Hosp, Dept Clin Lab, Lanzhou, Gansu, Peoples R China.

年份：2026

卷号：17

外文期刊名：FRONTIERS IN IMMUNOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001693020300001)】；

基金：The author(s) declared that financial support was received for this work and/or its publication. This work was supported by the Natural Science Foundation of Gansu Province (grant number: 23JRRA1282), the Innovation and Entrepreneurship Fund for Outstanding Graduate Students of the Gansu Provincial Department of Education (grant number: 2026CXCY-356), and the Intramural Research Fund of Gansu Provincial People's Hospital (grant number: 24GSSYH-5).

语种：英文

外文关键词：atherosclerosis; ferroptosis; heme oxygenase-1; oxidative stress; ROS

摘要：Atherosclerosis is the primary pathological basis of cardiovascular diseases, with macrophage dysfunction, lipid accumulation, and oxidative stress driving plaque formation and progression. Ferroptosis, an iron-dependent form of regulated cell death characterized by lipid peroxidation, has recently emerged as a pivotal mechanism influencing atherosclerosis. Heme oxygenase-1 (HO-1), a key regulator of heme catabolism and iron homeostasis, exerts dual roles in this process: moderate HO-1 activity confers cytoprotection through antioxidant effects, whereas excessive HO-1 expression promotes intracellular iron accumulation, oxidative stress, and ferroptotic cell death. In macrophages, HO-1 mediates both classical ferroptosis pathways via glutathione peroxidase 4 (GPX4) regulation and non-classical, erythrophagocytosis-induced ferroptosis, contributing to plaque instability. This review systematically examines the molecular mechanisms underlying HO-1-induced ferroptosis in atherosclerosis, emphasizing its interplay with iron metabolism, oxidative stress, and macrophage function. Understanding the context-dependent effects of HO-1 provides novel insights into the regulation of vascular cell fate and plaque stability, highlighting potential therapeutic targets for the prevention and treatment of atherosclerotic cardiovascular diseases.