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. 2021 Apr 12;8:649630. doi: 10.3389/fcvm.2021.649630

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Copyright © 2021 Choi and Kim.

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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CO inhibits pro-atherosclerotic processes. CO blocks the multifaceted signaling pathways related to atherosclerotic progress. This progress can include monocyte infiltration through adhesion molecules (i.e., ICAM-1 and VCAM-1), macrophage differentiation from monocytes, foam cell formation, and inflammatory cytokine releases and ONOO⁻ production. Additionally, CO reduces EC apoptosis and SMC migration and proliferation. OxLDL, oxidized low-density lipoprotein; ICAM-1, intercellular adhesion molecule-1; VCAM-1, vascular cell adhesion molecule-1; TNF-α, tumor necrosis factor-α; IL-1β, interleukin-1β.