Silencing of Non-POU-domain-containing octamer-binding protein stabilizes atherosclerotic plaque in apolipoprotein E-knockout mice via NF-κB signaling pathway

NonO may promote plaque destabilization and increase the incidence of plaque disruption in ApoE−/− mice by inducing the expression of inflammatory cytokines and matrix metalloproteinases and suppressing that of P4Hα1. The mechanism may involve the interaction of NonO with NF-κB leading to enhanced NF-κB nuclear translocation and phosphorylation.