Molecular Interactions Between Vascular Smooth Muscle Cells and Macrophages in Atherosclerosis

Figure 1. Summary of interactions involving an exchange of soluble factors between macrophages and VSMCs in atherosclerosis. Depiction of a vessel with an endothelial layer on the top and fibrous cap producing VSMCs lying underneath. Macrophage secretion of unestablished soluble factors, TNF-α, IL-5, and oxLDL mediated activation lead to transcriptional changes in VSMC. Solid arrows correspond to enhanced activity and dotted lines represent down regulated processes. Modifications result in increased monocyte recruitment, plaque instability, subendothelial calcification, and inflammation.

Figure 2. Transfer of atherosclerotic factors via extracellular vesicles. Macrophages transfer miRNA, LDL, and protein cocktails to other macrophages and VSMCs. The received content leads to changes in migration, motility, adhesion and phenotypic modulation.

Figure 3. 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.