{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T15:56:40Z","timestamp":1787932600818,"version":"build-2784847793"},"reference-count":95,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T00:00:00Z","timestamp":1770163200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100009620","name":"Science and Technology Department of Gansu Province","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100009620","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>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.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1737751","type":"journal-article","created":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T06:47:55Z","timestamp":1770187675000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["Reappraising heme oxygenase-1 as a ferroptosis modulator in atherosclerosis: a mechanism-focused review"],"prefix":"10.3389","volume":"17","author":[{"given":"Jia","family":"Xu","sequence":"first","affiliation":[{"name":"School of Public Health, Gansu University of Chinese Medicine","place":["Lanzhou, Gansu, 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