APOE and atherosclerosis: It was also revealed that in EC-specific progeroid mice overexpressing the dominant-negative form of TRF2 under the control of Tie2 or VE-cadherin promoter, SA-β-gal+ cells and the mRNA expression of cyclin-dependent kinase inhibitors (p16/INK4, p19/ARF, and p21/WAF-1) were increased in the lung endothelium, and atherosclerosis (lipid accumulation in the aorta and serum) was accelerated with target deletion of the apolipoprotein E (ApoE) gene [26].