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. 2022 May 20;9:857933. doi: 10.3389/fcvm.2022.857933

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Copyright © 2022 Ma, Ma, Shen, Wang, Bao, Liu, Ke and Qian.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A hypothetical scheme for the role of iron in ApoE deficiency-induced atherosclerosis. The increased iron accumulation in the aortic tissues (AET) may be mainly due to increased cell-iron uptake via IRP/TfR1 pathway. Increased ROS production, induced mainly by increased iron and possibly also partly by reduction in SOD and GSH-PX enzymes, plays an important role in endothelial activation and consequent monocyte recruitment to the arterial intimae, via up-regulation of the expression of cellular adhesion molecules ICAM1 and VCAM1, main ox-LDL receptor of endothelial cells LOX-1, important receptor for oxidized lipoproteins CD36, NF-κB phosphorylation, and pro-inflammatory cytokines TNFα, IL-1β, and IL-6, in the aortic tissues of mice.