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. 2021 Oct 15;8:737934. doi: 10.3389/fcvm.2021.737934

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Copyright © 2021 Beck-Joseph, Tabrizian and Lehoux.

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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Summary of interactions involving physical contact between macrophages and VSMCs in atherosclerosis. Arrows point in the direction of enhanced processes, and dotted lines indicate inhibition. CX3CL1/CX3CR1 interaction leads to increased VSMC accumulation and inflammation. ROS-mediated increase in VCAM1/ICAM1 and CCL2 result in enhanced subendothelial macrophage retention and monocyte recruitment, respectively. Fas-mediated VSMC-apoptosis and the influence of NO, TNF-α, and resistin on FAS-R/L surface expression.