FIGURE 8.

Schematic representation depicting the role of VTN in atherosclerotic plaque. The supply of sufficient VTN in the atherosclerotic plaque maintains stable conditions in the plaque, while chronic cholesterol load causing VTN downregulation induces a series of events which initiates inflammation leading to upregulation of NF‐κB, which in turn enhances ICAM‐1 and VCAM‐1 secretion. This leads to inflammatory cells build up and a shifting towards unresolved and chronic inflammation in the plaque mileu. In addition, MMPs are activated which leads to severe collagen degradation, resulting in an unstable plaque, indicating vulnerability towards acute events. Up arrow indicates upregulation and down arrow indicates down regulation. ICAM‐1, intracellular cell adhesion molecule‐1; MMPs, matrix metalloproteases; NF‐κB, nuclear factor kappa light chain enhancer of activated B cells; VCAM‐1, vascular cell adhesion molecule‐1; VSMC, vascular smooth muscle cells