Figure 6.

Synopsis of the putative functions attributed to CRP4 in atherosclerotic plaque initiation and progression. Proatherogenic CRP4 enhances plaque building by promoting the phenotypic switch and migratory properties of VSMCs. This results in a higher amount of α-SMA expression in the lesion area and an overall higher plaque burden. In advanced plaques, CRP4 may predominantly affect plaque stability through inhibition of the antioxidant enzyme PRDX4. Lower PRDX4 abundance in CRP4 proficient VSMCs and vessels causes a higher level of lesion oxLDL, and this is associated with an enhanced calcification. Vice versa, the anti-proliferative effects of CRP4 on VSMC/plaque cell proliferation may promote a vulnerable state of atherosclerotic plaques. However, the NC of ApoE^−/−/CRP4^+/+ lesions are smaller. Since no threshold above which a plaque becomes unstable has been determined, the significance of the latter finding remains unclear.