Atherosclerosis remains a significant global health challenge, arising from the complex interactions among dysregulated lipid metabolism, chronic inflammation and immune activation. Ferroptosis, marked by lipid peroxide buildup dependent on iron, is gaining recognition as a modulator of macrophage activity in atherosclerosis. Macrophages are the pivotal orchestrators of chronic inflammation and atherosclerotic plaque formation. The marked heterogeneity and plasticity of macrophages within plaques dynamically shape the local microenvironment, contributing to phenomena such as lipid overload, cytokine overactivation, hypoxia, and programmed cell death. This review examines how dysregulated iron handling, lipid metabolism, and redox imbalances synergise to induce macrophage ferroptosis in atherosclerosis. Moreover, ferroptosis contributes to the development and progression of atherosclerosis by causing dysfunction in vascular smooth muscle cells (VSMCs), vascular endothelial cells (VECs), and macrophages, thereby promoting plaque formation and instability. Furthermore, macrophages are intricately linked to ferroptosis, with this iron-dependent cell death enhancing oxidative stress and inflammatory pathways. Macrophage ferroptosis drives plaque progression and destabilisation, ultimately heightening the risk of rupture and cardiovascular events. By inhibiting macrophage ferroptosis, it may be possible to reduce oxidative stress and inflammation, stabilise atherosclerotic plaques, and ultimately lower the risk of cardiovascular events. This review highlights the therapeutic potential of targeting macrophage ferroptosis for the treatment of atherosclerosis.
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