Recognition and repair of 8-OH-dG lesions is carried out by the mitochondrial isoform, and we previously showed that Ogg1−/− BMDMs were more sensitive to menadione-induced mtDNA oxidative damage, and that inflammation caused by oxidized DNA damage and dyslipidemia-induced metabolic stress resulted in accelerated atherosclerosis in Ogg1−/−Ldlr−/− mice (22). This evidence concerns the gene OGG1 and metabolic syndrome.